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68 results on '"MESH: Kidney Diseases"'

1. Plasma Exchange and Glucocorticoids in Severe ANCA-Associated Vasculitis

Author

Lucy Smyth, Andrea Mazzetti, Charles D. Pusey, Lorraine Harper, Donna Reidlinger, Gina Gregorini, William F. Clark, Pexivas Investigators Pexivas Investigators, Adeera Levin, Toshiko Ito-Ihara, Chen-Au Peh, Xavier Puéchal, Ulrich Specks, Carmel M. Hawley, Oliver Floßmann, Simon Carette, Alina Casian, Wojciech Szczeklik, Peter A. Merkel, Janak de Zoysa, Nader Khalidi, David Jayne, Samir Mehta, Biljana Brezina, Ron Wald, Michael Walsh, Luis Felipe Flores-Suárez, Carol A. McAlear, L. Guillevin, Louis Girard, Natalie Ives, Wladimir Szpirt, Vladimir Tesar, Elizabeth Broadhurst, Christian Pagnoux, Shouichi Fujimoto, McMaster University [Hamilton, Ontario], Royal Adelaide Hospital [Adelaide Australia], Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), University of Miyazaki, McMaster University, St. Joseph’s Healthcare, Royal Berkshire Hospital, St. Michael's Hospital, University of British Columbia (UBC), Università degli Studi di Brescia [Brescia], Mount Sinai Hospital [Toronto, Canada] (MSH), Mayo Clinic [Rochester], Charles University [Prague] (CU), Instituto Nacional de Enfermedades Respiratorias [México, Mexico], University of Cambridge [UK] (CAM), Addenbrooke's Hospital, and Cambridge University NHS Trust

Subjects
MESH: Combined Modality Therapy, medicine.medical_specialty, Cyclophosphamide, medicine.medical_treatment, Azathioprine, 030204 cardiovascular system & hematology, urologic and male genital diseases, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, Gastroenterology, MESH: Dose-Response Relationship, Drug, MESH: Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, 03 medical and health sciences, 0302 clinical medicine, Maintenance therapy, immune system diseases, Internal medicine, Medicine, MESH: Incidence, cardiovascular diseases, 030212 general & internal medicine, skin and connective tissue diseases, Anti-neutrophil cytoplasmic antibody, MESH: Aged, MESH: Kidney Diseases, MESH: Middle Aged, MESH: Humans, business.industry, MESH: Cyclophosphamide, MESH: Adult, Glomerulonephritis, General Medicine, MESH: Plasma Exchange, medicine.disease, MESH: Induction Chemotherapy, MESH: Male, respiratory tract diseases, 3. Good health, MESH: Kidney Failure, Chronic, MESH: Administration, Oral, Rituximab, Plasmapheresis, MESH: Immunosuppressive Agents, MESH: Rituximab, MESH: Glucocorticoids, business, Vasculitis, MESH: Female, medicine.drug
Abstract

BACKGROUND More effective and safer treatments are needed for antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis. METHODS We conducted a randomized trial with a 2-by-2 factorial design to evaluate the use of plasma exchange and two regimens of oral glucocorticoids in patients with severe ANCA-associated vasculitis (defined by an estimated glomerular filtration rate of

Published
2020

2. Two cases of secondary AA amyloidosis involving the skin and chronic kidney infection with a nephrotic syndrome in a high-income country

Author

Florian Garo, Cedric Aglae, Olivier Moranne, Juliette Chatelain, Retiveau, Nolwenn, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Université de Montpellier (UM), Institut Desbrest de santé publique (IDESP), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)

Subjects
0301 basic medicine, medicine.medical_specialty, medicine.medical_treatment, Nephrotic syndrome, Renal function, Case Report, 030105 genetics & heredity, Kidney, Anasarca, Gastroenterology, 03 medical and health sciences, 0302 clinical medicine, AA amyloidosis, Internal medicine, MESH: Renal Insufficiency, Edema, Humans, Medicine, Renal medicine, MESH: Amyloidosis, Renal Insufficiency, Public health, MESH: Kidney Diseases, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, MESH: Humans, MESH: Middle Aged, business.industry, Amyloidosis, MESH: Kidney, General Medicine, Middle Aged, Skin ulcer, medicine.disease, Nephrectomy, MESH: Edema, medicine.anatomical_structure, Female, Kidney Diseases, MESH: Nephrotic Syndrome, medicine.symptom, business, MESH: Female, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, 030217 neurology & neurosurgery
Abstract

International audience; We present two French cases of amyloid-associated (AA) amyloidosis secondary to chronic infections. Patient 1, a 51-year-old heroin addict, was hospitalised for chest pain and anasarca. During hospitalisation, a nephrotic syndrome with an inflammatory condition was discovered along with a chronic skin ulcer on his arm. Salivary gland and kidney biopsies confirmed the diagnosis of AA amyloidosis. Renal function quickly declined and haemodialysis was initiated 6 months later. Patient 2, a 55-year-old woman, was hospitalised for obstructive pyelonephritis secondary to coraliform lithiasis. Renal insufficiency with an impure nephrotic syndrome was found. After nephrectomy due to chronic pyelonephritis and an atrophic cortex on the abdominal scan, the histology revealed AA amyloidosis. Despite treatment with ACE inhibitors and control of inflammation, the nephrotic syndrome persisted with rapid decline of the kidney function.

Published
2021

3. Gammapathie monoclonale en néphrologie : prévalence de l’atteinte rénale et facteurs prédictifs du résultat histologique

Author

Roux, Arthur, Université Paris Descartes - Faculté de Médecine (UPD5 Médecine), Université Paris Descartes - Paris 5 (UPD5), and Alexandre Karras

Subjects
Facteurs prédictifs, MESH: Kidney Diseases, MESH: MGRS, Gammapathie monoclonale, Néphropathie, MESH: Monoclonal Gammopathy, MESH: Kidney Biopsy, Biopsie rénale, Renal biopsy, MESH: Predictive Factors, MESH: Prevalence, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Prévalence
Abstract

Inroduction: the prevalence of monoclonal gammopathy (MG) and kidney disease increases with age. The nephrologist is often confronted with patients who have both circulating MG and kidney disease but do not know if these two events are related to each other. Methods : all patients who underwent renal biopsy in our center between July 2007 and July 2018 and had a GM were included to study the prevalence and identify predictors of nephropathy secondary to monoclonal gammopathy (NSMG). Results : of 2772 biopsied patients, 330 (12%) were included in the study. Nearly 80% of them had renal failure (GFR

Published
2019

4. In Reply to ‘Benefit of Eculizumab Compared to Standard of Care Still Unproven in C3 Glomerulopathy’

Author

Fadi Fakhouri, Moglie Le Quintrec, Véronique Frémeaux-Bacchi, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Service d'immunologie [HEGP, Paris], Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Centre de Recherche en Transplantation et Immunologie (U1064 Inserm - CRTI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), and Retiveau, Nolwenn

Subjects
medicine.medical_specialty, Standard of care, 030232 urology & nephrology, MEDLINE, 030204 cardiovascular system & hematology, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, 03 medical and health sciences, 0302 clinical medicine, Glomerulopathy, medicine, MESH: Glomerulonephritis, Membranoproliferative, MESH: Standard of Care, Intensive care medicine, ComputingMilieux_MISCELLANEOUS, MESH: Kidney Diseases, MESH: Humans, business.industry, Glomerulonephritis, Eculizumab, medicine.disease, [SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, MESH: Antibodies, Monoclonal, Humanized, Nephrology, Monoclonal, business, medicine.drug
Abstract

International audience

Published
2018

5. The safety of mineralocorticoid receptor antagonists (MRAs) in patients with heart failure

Author

Patrick Rossignol, Bertram Pitt, University of Michigan [Ann Arbor], University of Michigan System, Cardiovascular and Renal Clinical Trialists [Vandoeuvre-les-Nancy] (INI-CRCT), Institut Lorrain du Coeur et des Vaisseaux Louis Mathieu [Nancy], Défaillance Cardiovasculaire Aiguë et Chronique (DCAC), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), CIC-Nancy, Institut Lorrain du Coeur et des Vaisseaux Louis Mathieu [Nancy]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'investigation clinique [Nancy] (CIC), and Université de Lorraine (UL)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
medicine.medical_specialty, Hyperkalemia, Renal function, MESH: Hospitalization, MESH: Mineralocorticoid Receptor Antagonists, 030204 cardiovascular system & hematology, 03 medical and health sciences, Ventricular Dysfunction, Left, 0302 clinical medicine, Mineralocorticoid receptor, MESH: Practice Guidelines as Topic, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Internal medicine, MESH: Ventricular Dysfunction, Left, Medicine, Humans, MESH: Patient Selection, Pharmacology (medical), mineralocorticoid receptor antagonist, 030212 general & internal medicine, Dosing, ComputingMilieux_MISCELLANEOUS, Mineralocorticoid Receptor Antagonists, Heart Failure, MESH: Kidney Diseases, MESH: Humans, Ejection fraction, business.industry, Patient Selection, renal function, General Medicine, medicine.disease, 3. Good health, Hospitalization, Heart failure, MESH: Heart Failure, Inclusion and exclusion criteria, Practice Guidelines as Topic, Cardiology, MESH: Hyperkalemia, Kidney Diseases, medicine.symptom, business, MRAS
Abstract

Mineralocorticoid receptor antagonists (MRAs) have been accorded a class 1 indication for patients with chronic heart failure and a reduced left ventricular ejection fraction (HFREF) in both European and American guidelines. Uptake, however, has been less than optimal largely due to concerns about their safety, in particular the risk of hyperkalemia and renal dysfunction.This review presents the current state of affairs regarding the safety of MRAs in heart failure with reduced ejection fraction.Careful patient selection and adherence to guideline-recommended inclusion and exclusion criteria, dosing, and serial monitoring of serum potassium and renal function, along with patient education regarding the potassium content of common foods, should minimize these risks and allow increased use of MRAs. Additionally, this may also result in a further reduction in cardiovascular mortality and hospitalizations for heart failure. The development of new non-steroidal MRAs, and especially new potassium binding molecules that are well tolerated and effective, hold the promise for increased safety and, therefore, increased and more prolonged use of MRAs in patients with heart failure, especially those with chronic kidney disease, diabetes mellitus, and the elderly.

Published
2016

6. Metformin prevents experimental gentamicin-induced nephropathy by a mitochondria-dependent pathway

Author

Dominique Detaille, Elsa Briones, José M. López-Novoa, Xavier Leverve, Mohamad-Yehia El-Mir, Marta Prieto, Miguel Arévalo, Angel Puente, Ana I. Morales, Department of Physiology and Pharmacology, University of Salamanca, Department of Pharmacy and Pharmacological Technology, Department of Anatomy and Human Histology, Laboratoire de bioénergétique fondamentale et appliquée (LBFA), Université Joseph Fourier - Grenoble 1 (UJF)-Institut National de la Santé et de la Recherche Médicale (INSERM), Universidad de Salamanca, and Hamant, Sarah

Subjects
Male, MESH: Oxidation-Reduction, MESH: Acetylglucosaminidase, Apoptosis, 030204 cardiovascular system & hematology, Mitochondrion, Kidney, MESH: Metformin, medicine.disease_cause, Antioxidants, MESH: Lipid Peroxidation, Lipid peroxidation, chemistry.chemical_compound, 0302 clinical medicine, oxidative stress, MESH: Animals, chemistry.chemical_classification, 0303 health sciences, MESH: Oxidative Stress, biology, Cytochrome c, Cytochromes c, MESH: Reactive Oxygen Species, MESH: Cytochromes c, Metformin, 3. Good health, mitochondria, acute kidney injury, Nephrology, MESH: Permeability, Kidney Diseases, Oxidation-Reduction, medicine.drug, medicine.medical_specialty, MESH: Gentamicins, MESH: Rats, MESH: Mitochondria, Cytochrome c Group, gentamicin, Permeability, Nephrotoxicity, Electron Transport, 03 medical and health sciences, MESH: Hypoglycemic Agents, renal protection, Internal medicine, Acetylglucosaminidase, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, medicine, Animals, Hypoglycemic Agents, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Electron Transport, 030304 developmental biology, MESH: Kidney Diseases, Reactive oxygen species, MESH: Apoptosis, MESH: Antioxidants, Kidney metabolism, MESH: Kidney, MESH: Male, Rats, Endocrinology, chemistry, biology.protein, Lipid Peroxidation, Gentamicins, Reactive Oxygen Species, Oxidative stress, MESH: Cytochrome c Group
Abstract

International audience; The antidiabetic drug metformin can diminish apoptosis induced by oxidative stress in endothelial cells and prevent vascular dysfunction even in nondiabetic patients. Here we tested whether it has a beneficial effect in a rat model of gentamicin toxicity. Mitochondrial analysis, respiration intensity, levels of reactive oxygen species, permeability transition, and cytochrome c release were assessed 3 and 6 days after gentamicin administration. Metformin treatment fully blocked gentamicin-mediated acute renal failure. This was accompanied by a lower activity of N-acetyl-beta-D-glucosaminidase, together with a decrease of lipid peroxidation and increase of antioxidant systems. Metformin also protected the kidney from histological damage 6 days after gentamicin administration. These in vivo markers of kidney dysfunction and their correction by metformin were complemented by in vitro studies of mitochondrial function. We found that gentamicin treatment depleted respiratory components (cytochrome c, NADH), probably due to the opening of mitochondrial transition pores. These injuries, partly mediated by a rise in reactive oxygen species from the electron transfer chain, were significantly decreased by metformin. Thus, our study suggests that pleiotropic effects of metformin can lessen gentamicin nephrotoxicity and improve mitochondrial homeostasis.

Published
2010

7. Kidney protection by hypothermic total liquid ventilation after cardiac arrest in rabbits

Author

Tissier, Renaud, Giraud, Sebastien, Quellard, Nathalie, Fernandez, Béatrice, Lidouren, Fanny, Darbera, Lys, Kohlhauer, Matthias, Pons, Sandrine, Chenoune, Mourad, Bruneval, Patrick, Goujon, Jean-Michel, Ghaleh, Bijan, Berdeaux, Alain, Hauet, Thierry, INSERM U955, équipe 3, Pharmacie-Toxicologie, École nationale vétérinaire - Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-École nationale vétérinaire - Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Poitiers, Service de Biochimie [Poitiers], Centre hospitalier universitaire de Poitiers (CHU Poitiers), Laboratoire de Recherche en Imagerie : Méthodes d'imagerie des Échanges transcapillaires (LRI - EA4062), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), École nationale vétérinaire - Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), This study was supported by a grant (ABYSS- R12031JJ) from the 'Agence Nationale pour la Recherche' (Paris, France). It was also suported by Inserm, Université de Poitiers, Région Poitou-Charentes, Conseil général de la Vienne, Région Ile-de-France (CODDIM), University Paris Est Créteil and CHU de Poitiers. R. Tissier was a recipient of a 'Contrat d'Interface Inserm- ENV'. M. Kohlhauer was supported by a doctoral fellowship from the 'Region Ile-de France'., and Guellaen, Georges

Subjects
MESH: Heart Arrest, MESH: Kidney Diseases, MESH: Hypothermia, Induced, MESH: Liquid Ventilation, MESH: Kidney Function Tests, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Rabbits, MESH: Animals, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Kidney, MESH: Disease Models, Animal, MESH: Treatment Outcome
Abstract

International audience; BACKGROUND: Total liquid ventilation (TLV) with perfluorocarbons has been shown to induce rapid protective cooling in animal models of myocardial ischemia and cardiac arrest, with improved neurological and cardiovascular outcomes after resuscitation. In this study, the authors hypothesized that hypothermic TLV can also limit kidney injury after cardiac arrest. METHODS: Anesthetized rabbits were submitted to 15 min of untreated ventricular fibrillation. After resuscitation, three groups of eight rabbits each were studied such as (1) life support plus hypothermia (32°-33 °C) induced by cold TLV (TLV group), (2) life support without hypothermia (control group), and (3) Sham group (no cardiac arrest). Life support was continued for 6 h before euthanasia and kidney removal. RESULTS: Time to target esophageal temperature was less than 5 min in the TLV group. Hypothermia was accompanied by preserved renal function in the TLV group as compared with control group regarding numerous markers including creatinine blood levels (12 ± 1 vs. 16 ± 2 mg/l, respectively; mean ± SEM), urinary N-acetyl-β-(D)-glucosaminidase (1.70 ± 0.11 vs. 3.07 ± 0.10 U/mol of creatinine), γ-glutamyltransferase (8.36 ± 0.29 vs. 12.96 ± 0.44 U/mol of creatinine), or β2-microglobulin (0.44 ± 0.01 vs. 1.12 ± 0.04 U/mol of creatinine). Kidney lesions evaluated by electron microscopy and conventional histology were also attenuated in TLV versus control groups. The renal-protective effect of TLV was not related to differences in delayed inflammatory or immune renal responses because transcriptions of, for example, interferon-γ, tumor necrosis factor-α, interleukin-1β, monocyte chemoattractant protein-1, toll-like receptor-2, toll-like receptor-4, and vascular endothelial growth factor were similarly altered in TLV and control versus Sham. CONCLUSION: Ultrafast cooling with TLV is renal protective after cardiac arrest and resuscitation, which could increase kidney availability for organ donation.

Published
2014

8. Kidney protection by hypothermic total liquid ventilation after cardiac arrest in rabbits

Author

Tissier , Renaud, Giraud , Sebastien, Quellard , Nathalie, Fernandez , Béatrice, Lidouren , Fanny, Darbera , Lys, Kohlhauer , Matthias, Pons , Sandrine, Chenoune , Mourad, Bruneval , Patrick, Goujon , Jean-Michel, Ghaleh , Bijan, Berdeaux , Alain, Hauet , Thierry, INSERM U955, équipe 3, Pharmacie-Toxicologie, École nationale vétérinaire d'Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-École nationale vétérinaire d'Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Poitiers, Service de Biochimie [Poitiers], Centre hospitalier universitaire de Poitiers (CHU Poitiers), Laboratoire de Recherche en Imagerie : Méthodes d'imagerie des Échanges transcapillaires (LRI - EA4062), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Descartes - Paris 5 (UPD5), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), École nationale vétérinaire d'Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), This study was supported by a grant (ABYSS- R12031JJ) from the 'Agence Nationale pour la Recherche' (Paris, France). It was also suported by Inserm, Université de Poitiers, Région Poitou-Charentes, Conseil général de la Vienne, Région Ile-de-France (CODDIM), University Paris Est Créteil and CHU de Poitiers. R. Tissier was a recipient of a 'Contrat d'Interface Inserm- ENV'. M. Kohlhauer was supported by a doctoral fellowship from the 'Region Ile-de France'., Ecole Nationale Vétérinaire d'Alfort-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ) -Ecole Nationale Vétérinaire d'Alfort-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ) -Institut Mondor de Recherche Biomédicale ( IMRB ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -IFR10, Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT ), Université de Poitiers-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Centre hospitalier universitaire de Poitiers ( CHU Poitiers ), Laboratoire de Recherche en Imagerie : Méthodes d'imagerie des Échanges transcapillaires ( LRI - EA4062 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut Mondor de Recherche Biomédicale ( IMRB ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), and Ecole Nationale Vétérinaire d'Alfort-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 )

Subjects
MESH: Heart Arrest, MESH: Kidney Diseases, MESH : Heart Arrest, MESH: Hypothermia, Induced, MESH: Liquid Ventilation, MESH : Kidney Function Tests, MESH: Rabbits, MESH : Liquid Ventilation, MESH : Treatment Outcome, MESH: Kidney, MESH : Disease Models, Animal, MESH : Kidney, MESH: Kidney Function Tests, MESH : Kidney Diseases, MESH : Rabbits, MESH: Animals, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH : Animals, MESH: Disease Models, Animal, [ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH : Hypothermia, Induced, MESH: Treatment Outcome
Abstract

International audience; BACKGROUND: Total liquid ventilation (TLV) with perfluorocarbons has been shown to induce rapid protective cooling in animal models of myocardial ischemia and cardiac arrest, with improved neurological and cardiovascular outcomes after resuscitation. In this study, the authors hypothesized that hypothermic TLV can also limit kidney injury after cardiac arrest. METHODS: Anesthetized rabbits were submitted to 15 min of untreated ventricular fibrillation. After resuscitation, three groups of eight rabbits each were studied such as (1) life support plus hypothermia (32°-33 °C) induced by cold TLV (TLV group), (2) life support without hypothermia (control group), and (3) Sham group (no cardiac arrest). Life support was continued for 6 h before euthanasia and kidney removal. RESULTS: Time to target esophageal temperature was less than 5 min in the TLV group. Hypothermia was accompanied by preserved renal function in the TLV group as compared with control group regarding numerous markers including creatinine blood levels (12 ± 1 vs. 16 ± 2 mg/l, respectively; mean ± SEM), urinary N-acetyl-β-(D)-glucosaminidase (1.70 ± 0.11 vs. 3.07 ± 0.10 U/mol of creatinine), γ-glutamyltransferase (8.36 ± 0.29 vs. 12.96 ± 0.44 U/mol of creatinine), or β2-microglobulin (0.44 ± 0.01 vs. 1.12 ± 0.04 U/mol of creatinine). Kidney lesions evaluated by electron microscopy and conventional histology were also attenuated in TLV versus control groups. The renal-protective effect of TLV was not related to differences in delayed inflammatory or immune renal responses because transcriptions of, for example, interferon-γ, tumor necrosis factor-α, interleukin-1β, monocyte chemoattractant protein-1, toll-like receptor-2, toll-like receptor-4, and vascular endothelial growth factor were similarly altered in TLV and control versus Sham. CONCLUSION: Ultrafast cooling with TLV is renal protective after cardiac arrest and resuscitation, which could increase kidney availability for organ donation.

Published
2014

9. Le syndrome des antiphospholipides en néphrologie. Atteinte rénale et aspects pratiques de la prise en charge

Author

Dekeyser, Manon, Zuily, Stéphane, Champigneulle, Jacqueline, Eschwège, Valérie, Frimat, Luc, Perret-Guillaume, Christine, Wahl, Denis, Service de néphrologie-hémodialyse-transplantation [CHRU Nancy], Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Défaillance Cardiovasculaire Aiguë et Chronique (DCAC), Université de Lorraine (UL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Centre régional de compétence des Maladies systémiques et auto-immunes rares de l'adulte et Maladies vasculaires rares, Service d’Anatomie Pathologique [CHRU Nancy], Service d'Hématologie Biologique [CHRU Nancy], Maladies chroniques, santé perçue, et processus d'adaptation (APEMAC), Université Paris Descartes - Paris 5 (UPD5)-Université de Lorraine (UL), Service de Gérontologie [CHRU Nancy], and Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL)

Subjects
Biopsy, Renal Veins, MESH: Kidney Transplantation, MESH: Biopsy, Renal Artery, Antiphospholipid syndrome, Thrombophilia, MESH: Renal Dialysis, Traitement, Dialyse, MESH: Middle Aged, MESH: Arterial Occlusive Diseases, Disease Management, Middle Aged, Cardiovascular Diseases, MESH: Platelet Aggregation Inhibitors, MESH: Renal Circulation, Female, Kidney Diseases, Arterial Occlusive Diseases, MESH: Anticoagulants, MESH: Disease Management, MESH: Nervous System Diseases, MESH: Renal Artery, Renal Circulation, Renal Dialysis, MESH: Antiphospholipid Syndrome, Humans, MESH: Thrombosis, MESH: Contraindications, Antihypertensive Agents, MESH: Thrombocytopenia, Transplantation, MESH: Antihypertensive Agents, MESH: Kidney Diseases, MESH: Humans, Thrombotic Microangiopathies, Contraindications, MESH: Thrombotic Microangiopathies, MESH: Thrombophilia, Anticoagulants, MESH: Cardiovascular Diseases, Thrombosis, Kidney Transplantation, Thrombocytopenia, Néphropathie associée au syndrome des antiphospholipides, Treatment, MESH: Renal Veins, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Nervous System Diseases, Dialysis, MESH: Female, Platelet Aggregation Inhibitors, Syndrome des antiphospholipides, Antiphospholipid syndrome nephropathy
Abstract

International audience; The antiphospholipid syndrome is a thrombophilia characterized by the combination of arterial and/or venous thrombotic events or obstetric clinical events, associated with persistent presence of antiphospholipid antibodies. In this syndrome, thromboses may affect all of the vascular tree, renal damage is frequently associated with a specific antiphospholipid syndrome nephropathy. We propose in this review to provide updated recommendations on the management of antiphospholipid syndrome in nephrology. Treatment is based on long-term anticoagulant therapy with or without antiplatelet agents according to clinical events. The use of a conventional nephroprotection must not be forgotten (strict control of blood pressure with drugs blocking the renin-angiotensin-aldosterone system). Catastrophic antiphospholipid syndrome is an extremely severe complication which can threaten the vital prognosis of the patient. This justifies particular surveillance, as well as prevention in high-risk situations. We also illustrate the difficulties of long-term management in these patients, both in dialysis or kidney transplantation.; Le syndrome des antiphospholipides est une thrombophilie caractérisée par l’association d’un événement clinique thrombotique (artériel et/ou veineux) ou obstétrical, associé à la présence durable d’anticorps antiphospholipides. L’atteinte pouvant toucher l’ensemble de l’arbre vasculaire, une atteinte rénale est fréquemment associée avec la description maintenant bien codifiée de la néphropathie associée au syndrome des antiphospholipides. Nous proposons dans cette revue des recommandations actualisées sur la prise en charge du syndrome des antiphospholipides en néphrologie. La thérapeutique se base sur une anticoagulation plus ou moins une antiagrégation à long terme en fonction des événements cliniques sans oublier le recours à une néphroprotection classique (contrôle strict de la pression artérielle avec notamment des thérapeutiques bloquant le système rénine–angiotensine–aldostérone). Le syndrome catastrophique des antiphospholipides est une complication extrêmement grave pouvant mettre en jeu le pronostic vital du patient. Celui-ci justifie une attention toute particulière, ainsi qu’une prévention dans les situations à risque. Nous illustrons également les difficultés de prise en charge au long cours de ces patients, tant en dialyse qu’en transplantation rénale.

Published
2014

10. How I treat monoclonal gammopathy of renal significance (MGRS)

Author

Fermand, Jean-Paul, Bridoux, Franck, Kyle, Robert A, Kastritis, Efstathios, Weiss, Brendan M, Cook, Mark A, Drayson, Mark T, Dispenzieri, Angela, Leung, Nelson, Renseigné, Non, Service d'hématologie clinique et de thérapie cellulaire [CHU Saint-Antoine], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Saint-Antoine [APHP], Service de néphrologie - hémodialyse et transplantation rénale, Centre hospitalier universitaire de Poitiers (CHU Poitiers), Contrôle de la Réponse Immune B et des Lymphoproliférations (CRIBL), Centre National de la Recherche Scientifique (CNRS)-Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)

Subjects
Pathology, medicine.medical_specialty, MESH: Cryoglobulinemia, Immunology, 030232 urology & nephrology, Paraproteinemias, Biochemistry, Immunoglobulin Light-chain Amyloidosis, 03 medical and health sciences, 0302 clinical medicine, MESH: Paraproteinemias, MESH: B-Lymphocytes, medicine, Humans, MESH: Amyloidosis, Kidney transplantation, Multiple myeloma, MESH: Fanconi Syndrome, Kidney, B-Lymphocytes, MESH: Kidney Diseases, MESH: Humans, business.industry, Cell Biology, Hematology, Amyloidosis, medicine.disease, Fanconi Syndrome, 3. Good health, medicine.anatomical_structure, Cryoglobulinemia, 030220 oncology & carcinogenesis, Monoclonal, [SDV.IMM]Life Sciences [q-bio]/Immunology, Kidney Diseases, business, Monoclonal gammopathy of undetermined significance, Monoclonal Immunoglobulin Deposition Disease, Kidney disease
Abstract

Recently, the term monoclonal gammopathy of renal significance (MGRS) was introduced to distinguish monoclonal gammopathies that result in the development of kidney disease from those that are benign. By definition, patients with MGRS have B-cell clones that do not meet the definition of multiple myeloma or lymphoma. Nevertheless, these clones produce monoclonal proteins that are capable of injuring the kidney resulting in permanent damage. Except for immunoglobulin light chain amyloidosis with heart involvement in which death can be rapid, treatment of MGRS is often indicated more to preserve kidney function and prevent recurrence after kidney transplantation rather than the prolongation of life. Clinical trials are rare for MGRS-related kidney diseases, except in immunoglobulin light chain amyloidosis. Treatment recommendations are therefore based on the clinical data obtained from treatment of the clonal disorder in its malignant state. The establishment of these treatment recommendations is important until data can be obtained by clinical trials of MGRS-related kidney diseases.

Published
2013

11. Kidney protection by hypothermic total liquid ventilation after cardiac arrest in rabbits

Author

Mourad Chenoune, Alain Berdeaux, Sébastien Giraud, Fanny Lidouren, Matthias Kohlhauer, Jean-Michel Goujon, Lys Darbera, Renaud Tissier, Patrick Bruneval, Bijan Ghaleh, Thierry Hauet, Nathalie Quellard, Béatrice Fernandez, Sandrine Pons, INSERM U955, équipe 3, Pharmacie-Toxicologie, École nationale vétérinaire - Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-École nationale vétérinaire - Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Poitiers, Service de Biochimie [Poitiers], Centre hospitalier universitaire de Poitiers (CHU Poitiers), Laboratoire de Recherche en Imagerie : Méthodes d'imagerie des Échanges transcapillaires (LRI - EA4062), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), École nationale vétérinaire - Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), This study was supported by a grant (ABYSS- R12031JJ) from the 'Agence Nationale pour la Recherche' (Paris, France). It was also suported by Inserm, Université de Poitiers, Région Poitou-Charentes, Conseil général de la Vienne, Région Ile-de-France (CODDIM), University Paris Est Créteil and CHU de Poitiers. R. Tissier was a recipient of a 'Contrat d'Interface Inserm- ENV'. M. Kohlhauer was supported by a doctoral fellowship from the 'Region Ile-de France'., École nationale vétérinaire d'Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-École nationale vétérinaire d'Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-Institut Mondor de Recherche Biomédicale (IMRB), Université de Poitiers-Institut National de la Santé et de la Recherche Médicale (INSERM), and École nationale vétérinaire d'Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)

Subjects
Resuscitation, MESH: Heart Arrest, Myocardial ischemia, Liquid Ventilation, Renal function, MESH: Rabbits, 030204 cardiovascular system & hematology, Kidney, Kidney Function Tests, Article, 03 medical and health sciences, 0302 clinical medicine, Hypothermia, Induced, medicine, Animals, MESH: Animals, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Treatment Outcome, MESH: Kidney Diseases, MESH: Hypothermia, Induced, MESH: Liquid Ventilation, business.industry, 030208 emergency & critical care medicine, MESH: Kidney, Hypothermia, 3. Good health, Heart Arrest, Disease Models, Animal, Anesthesiology and Pain Medicine, medicine.anatomical_structure, Treatment Outcome, MESH: Kidney Function Tests, Anesthesia, Total Liquid Ventilation, Hypot, Kidney Diseases, Rabbits, medicine.symptom, MESH: Disease Models, Animal, business, Cardiovascular outcomes
Abstract

Background: Total liquid ventilation (TLV) with perfluorocarbons has been shown to induce rapid protective cooling in animal models of myocardial ischemia and cardiac arrest, with improved neurological and cardiovascular outcomes after resuscitation. In this study, the authors hypothesized that hypothermic TLV can also limit kidney injury after cardiac arrest. Methods: Anesthetized rabbits were submitted to 15 min of untreated ventricular fibrillation. After resuscitation, three groups of eight rabbits each were studied such as (1) life support plus hypothermia (32°–33°C) induced by cold TLV (TLV group), (2) life support without hypothermia (control group), and (3) Sham group (no cardiac arrest). Life support was continued for 6 h before euthanasia and kidney removal. Results: Time to target esophageal temperature was less than 5 min in the TLV group. Hypothermia was accompanied by preserved renal function in the TLV group as compared with control group regarding numerous markers including creatinine blood levels (12 ± 1 vs. 16 ± 2 mg/l, respectively; mean ± SEM), urinary N-acetyl-β-(d)-glucosaminidase (1.70 ± 0.11 vs. 3.07 ± 0.10 U/mol of creatinine), γ-glutamyltransferase (8.36 ± 0.29 vs. 12.96 ± 0.44 U/mol of creatinine), or β2-microglobulin (0.44 ± 0.01 vs. 1.12 ± 0.04 U/mol of creatinine). Kidney lesions evaluated by electron microscopy and conventional histology were also attenuated in TLV versus control groups. The renal-protective effect of TLV was not related to differences in delayed inflammatory or immune renal responses because transcriptions of, for example, interferon-γ, tumor necrosis factor-α, interleukin-1β, monocyte chemoattractant protein-1, toll-like receptor-2, toll-like receptor-4, and vascular endothelial growth factor were similarly altered in TLV and control versus Sham. Conclusion: Ultrafast cooling with TLV is renal protective after cardiac arrest and resuscitation, which could increase kidney availability for organ donation.

Published
2013

12. Role of CFTR in oxidative stress and suicidal death of renal cells during cisplatin-induced nephrotoxicity

Author

Marc Cougnon, Isabelle Rubera, Baharia Mograbi, Nicolas Melis, Christophe Duranton, Michel Tauc, Physiologie cellulaire et moléculaire des systèmes intégrés (PCMSI), Université Nice Sophia Antipolis (... - 2019) (UNS), and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)

Subjects
MESH: Cell Death, Cancer Research, [SDV]Life Sciences [q-bio], Intracellular Space, Cystic Fibrosis Transmembrane Conductance Regulator, Pharmacology, Kidney, medicine.disease_cause, Benzoates, Kidney Tubules, Proximal, DNA Adducts, Mice, 0302 clinical medicine, MESH: Caspase 3, MESH: Animals, NGAL, chemistry.chemical_classification, MESH: Glutathione, MESH: Cystic Fibrosis Transmembrane Conductance Regulator, 0303 health sciences, MESH: Oxidative Stress, Cell Death, biology, Caspase 3, apoptosis, MESH: Reactive Oxygen Species, respiratory system, Glutathione, Cystic fibrosis transmembrane conductance regulator, 3. Good health, medicine.anatomical_structure, Biochemistry, MESH: Cell Survival, 030220 oncology & carcinogenesis, kidney injury, Thiazolidines, MESH: Intracellular Space, Original Article, Female, Kidney Diseases, MESH: Thiazolidines, Intracellular, MESH: DNA Adducts, medicine.drug, MESH: Enzyme Activation, MESH: Cell Line, Tumor, MESH: Rats, Cell Survival, Immunology, Nephrotoxicity, 03 medical and health sciences, Cellular and Molecular Neuroscience, CFTRinh-172, MESH: Kidney Tubules, Proximal, Cell Line, Tumor, GSH, medicine, cancer, Animals, Humans, Rats, Wistar, MESH: Mice, Platinum, 030304 developmental biology, Cisplatin, Reactive oxygen species, MESH: Kidney Diseases, MESH: Humans, Body Weight, MESH: Platinum, Cell Biology, MESH: Kidney, MESH: Rats, Wistar, MESH: Benzoates, Rats, respiratory tract diseases, MESH: Body Weight, Enzyme Activation, Oxidative Stress, chemistry, MESH: Cisplatin, Apoptosis, biology.protein, MESH: Biomarkers, Reactive Oxygen Species, MESH: Female, Biomarkers, Oxidative stress
Abstract

International audience; The clinical use of the antineoplastic drug cisplatin is limited by its deleterious nephrotoxic side effect. Cisplatin-induced nephrotoxicity is associated with an increase in oxidative stress, leading ultimately to renal cell death and irreversible kidney dysfunction. Oxidative stress could be modified by the cystic fibrosis transmembrane conductance regulator protein (CFTR), a Cl(-) channel not only involved in chloride secretion but as well in glutathione (GSH) transport. Thus, we tested whether the inhibition of CFTR could protect against cisplatin-induced nephrotoxicity. Using a renal proximal cell line, we show that the specific inhibitor of CFTR, CFTR(inh)-172, prevents cisplatin-induced cell death and apoptosis by modulating the intracellular reactive oxygen species balance and the intracellular GSH concentration. This CFTR(inh)-172-mediated protective effect occurs without affecting cellular cisplatin uptake or the formation of platinum-DNA adducts. The protective effect of CFTR(inh)-172 in cisplatin-induced nephrotoxicity was also investigated in a rat model. Five days after receiving a single cisplatin injection (5 mg/kg), rats exhibited renal failure, as evidenced by the alteration of biochemical and functional parameters. Pretreatment of rats with CFTR(inh)-172 (1 mg/kg) prior to cisplatin injection significantly prevented these deleterious cisplatin-induced nephrotoxic effects. Finally, we demonstrate that CFTR(inh)-172 does not impair cisplatin-induced cell death in the cisplatin-sensitive A549 cancer cell line. In conclusion, the use of a specific inhibitor of CFTR may represent a novel therapeutic approach in the prevention of nephrotoxic side effects during cisplatin treatment without affecting its antitumor efficacy.

Published
2013

13. [Renal urinary shear stress: a novel actor in nephropathies]

Author

Gonzalez, Julien, Essig, Marie, Klein, Julie, Caubet, Cécile, Dissard, Romain, Bascands, Jean-Loup, Schanstra, Joost P, Buffin-Meyer, Bénédicte, Pharmacologie des Immunosuppresseurs et de la Transplantation (PIST), Université de Limoges (UNILIM)-CHU Limoges-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), and Simon, Marie Francoise

Subjects
MESH: Cell Differentiation, MESH: Kidney Diseases, Polycystic Kidney Diseases, MESH: Humans, Cell Differentiation, Urine, [SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, MESH: Urine, Kidney Tubules, MESH: Rheology, MESH: Cytoskeleton, MESH: Kidney Tubules, Animals, Humans, MESH: Animals, Kidney Diseases, Rheology, Cytoskeleton, MESH: Polycystic Kidney Diseases
Abstract

International audience; The role of fluid shear stress is well established in vascular pathophysiology. However, urinary shear stress now also appears as a key mechanism in the regulation of renal function. In addition, there is a growing body of evidence showing that modified urinary shear stress is involved in the development of nephropathies. Therefore we review here the state-of-the-art on the pathophysiological roles of urinary shear stress.

Published
2013

14. Monoclonal gammopathy of renal significance: when MGUS is no longer undetermined or insignificant

Author

Leung, Nelson, Bridoux, Franck, Hutchison, Colin A, Nasr, Samih H, Cockwell, Paul, Fermand, Jean-Paul, Dispenzieri, Angela, Song, Kevin W, Kyle, Robert A, Renseigné, Non, Contrôle de la Réponse Immune B et des Lymphoproliférations (CRIBL), Centre National de la Recherche Scientifique (CNRS)-Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503), Service de néphrologie - hémodialyse et transplantation rénale, Centre hospitalier universitaire de Poitiers (CHU Poitiers), Service d'hématologie clinique et de thérapie cellulaire [CHU Saint-Antoine], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Saint-Antoine [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)

Subjects
Pathology, medicine.medical_specialty, Immunology, Paraproteinemias, 030232 urology & nephrology, Renal function, MESH: Antineoplastic Agents, Alkylating, Monoclonal Gammopathy of Undetermined Significance, Biochemistry, MESH: Kidney Transplantation, 03 medical and health sciences, 0302 clinical medicine, MESH: Paraproteinemias, medicine, Humans, Antineoplastic Agents, Alkylating, Multiple myeloma, Kidney transplantation, Kidney, MESH: Kidney Diseases, MESH: Humans, business.industry, Cell Biology, Hematology, medicine.disease, Kidney Transplantation, 3. Good health, medicine.anatomical_structure, MESH: Kidney Failure, Chronic, 030220 oncology & carcinogenesis, MESH: Monoclonal Gammopathy of Undetermined Significance, Monoclonal, Disease Progression, Kidney Failure, Chronic, [SDV.IMM]Life Sciences [q-bio]/Immunology, Kidney Diseases, MESH: Disease Progression, Clone (B-cell biology), business, Monoclonal gammopathy of undetermined significance, Monoclonal Immunoglobulin Deposition Disease
Abstract

Multiple myeloma is the most frequent monoclonal gammopathy to involve the kidney; however, a growing number of kidney diseases associated with other monoclonal gammopathies are being recognized. Although many histopathologic patterns exist, they are all distinguished by the monoclonal immunoglobulin (or component) deposits. The hematologic disorder in these patients is more consistent with monoclonal gammopathy of undetermined significance (MGUS) than with multiple myeloma. Unfortunately, due to the limitations of the current diagnostic schema, they are frequently diagnosed as MGUS. Because treatment is not recommended for MGUS, appropriate therapy is commonly withheld. In addition to end-stage renal disease, the persistence of the monoclonal gammopathy is associated with high rates of recurrence after kidney transplantation. Preservation and restoration of kidney function are possible with successful treatment targeting the responsible clone. Achievement of hematologic complete response has been shown to prevent recurrence after kidney transplantation. There is a need for a term that properly conveys the pathologic nature of these diseases. We think the term monoclonal gammopathy of renal significance is most helpful to indicate a causal relationship between the monoclonal gammopathy and the renal damage and because the significance of the monoclonal gammopathy is no longer undetermined.

Published
2012

15. Fanconi syndrome and chronic kidney disease in paroxysmal nocturnal hemoglobinuria: effect of eculizumab therapy

Author

Nathalie Quellard, Sébastien Delbès, Edouard Randriamalala, Simohamed Belmouaz, Eric Moumas, Guy Touchard, Franck Bridoux, Fannie Leroy, Estelle Desport, Brigitte Dreyfus, Contrôle de la Réponse Immune B et des Lymphoproliférations (CRIBL), Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Centre National de la Recherche Scientifique (CNRS), Service de néphrologie - hémodialyse et transplantation rénale, Centre hospitalier universitaire de Poitiers (CHU Poitiers), and Carrion, Claire

Subjects
Male, Hemoglobinuria, Paroxysmal, 030232 urology & nephrology, Gastroenterology, 0302 clinical medicine, hemic and lymphatic diseases, MESH: Fanconi Syndrome, MESH: Aged, Kidney, MESH: Middle Aged, MESH: Hemoglobinuria, Paroxysmal, 05 social sciences, General Medicine, Middle Aged, Eculizumab, 3. Good health, medicine.anatomical_structure, Nephrology, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Kidney Diseases, Hemoglobinuria, medicine.drug, medicine.medical_specialty, [SDV.IMM] Life Sciences [q-bio]/Immunology, Renal function, Antibodies, Monoclonal, Humanized, 03 medical and health sciences, Internal medicine, 0502 economics and business, medicine, Humans, Aged, MESH: Kidney Diseases, MESH: Humans, business.industry, MESH: Chronic Disease, Fanconi syndrome, Fanconi Syndrome, medicine.disease, MESH: Male, Endocrinology, MESH: Antibodies, Monoclonal, Humanized, Hemosiderin, Chronic Disease, Paroxysmal nocturnal hemoglobinuria, 050211 marketing, business, MESH: Female, Kidney disease
Abstract

International audience; The association of Fanconi syndrome (FS) and chronic kidney disease (CKD) has been rarely described during the course of paroxysmal nocturnal hemoglobinuria (PNH). We report 2 patients with PNH and CKD associated with proximal tubule dysfunction, which manifested as full-blown FS in one case. In both patients, abnormal iron load within the kidneys was demonstrated by magnetic resonance imaging, which correlated with diffuse and numerous hemosiderin inclusions within proximal tubular cells. After 12 months, eculizumab treatment resulted in significant decrease in the kidney iron load in both cases. Glomerular filtration rate improved in one case and was stabilized in the other, in whom pretreatment kidney biopsy had shown severe extensive interstitial fibrosis. However, symptoms of proximal tubular dysfunction persisted in both patients. These data suggest that hemosiderin deposition in proximal tubules is probably an important mechanism involved in the development of FS, an under recognized and early manifestation of CKD in PNH. Prolonged treatment with eculizumab may improve long-term renal function in PNH patients with CKD.

Published
2012

16. The KUPKB: a novel Web application to access multiomics data on kidney disease

Author

Jean-Loup Bascands, Aristidis Charonis, Simon Jupp, Rana Chaaya, Julie Klein, Joost P. Schanstra, Panagiotis Moulos, Robert Stevens, Bénédicte Buffin-Meyer, Myriem Fernandez, Audrey Casemayou, School of Computer Science [Manchester], University of Manchester [Manchester], Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Infections Parasitaires : Transmission, Physiopathologie et Thérapeutiques (IP-TPT), Service de Santé des Armées-Assistance Publique - Hôpitaux de Marseille (APHM)-Aix Marseille Université (AMU)-Institut de Recherche pour le Développement (IRD), Section of Histology, Biomedical Research Foundation of the Academy of Athens-Center for Basic Research I-Foundation of the Academy of Athens, Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de Recherche pour le Développement (IRD)-Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)-Service de Santé des Armées, and Simon, Marie Francoise

Subjects
Male, Databases, Factual, MESH: Rats, MESH: Calreticulin, In silico, 030232 urology & nephrology, Genomics, Context (language use), MESH: Rats, Sprague-Dawley, Biology, Bioinformatics, Proteomics, Biochemistry, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, Genetics, medicine, Web application, Animals, Humans, MESH: Animals, Molecular Biology, 030304 developmental biology, 0303 health sciences, Internet, MESH: Kidney Diseases, MESH: Humans, business.industry, MESH: Immunohistochemistry, medicine.disease, Omics, Immunohistochemistry, MESH: Databases, Factual, MESH: Male, 3. Good health, Rats, Disease Models, Animal, MESH: Internet, Knowledge base, Kidney Diseases, MESH: Disease Models, Animal, business, Calreticulin, Biotechnology, Kidney disease
Abstract

International audience; The information gathered from the large number of omics experiments in renal biology is underexplored, as it is scattered over many publications or held in supplemental data. To address this, we have developed an open-source Kidney and Urinary Pathway Knowledge Base (KUPKB) that facilitates simple exploration of these omics data. The KUPKB currently comprises 220 data sets (miRNA, mRNA, proteins, and metabolites) extracted from existing publications or databases. Researchers can explore the integrated data using the iKUP browser, and a simple template is provided to submit new omics data sets to the knowledge base. As an example of iKUP's use, we show how we identified, in silico, calreticulin as a protein induced in human interstitial fibrosis and tubular atrophy (IFTA) in chronic kidney transplant rejection; a link that would have been difficult to establish using existing Web-based tools. Using immunohistochemistry, we validated in vivo this in silico result in human and rat biopsies of IFTA, thus identifying calreticulin as a potential new player in chronic kidney transplant rejection. The KUPKB provides a simple tool that enables users to quickly survey a wide range of omics data sets and has been shown to facilitate rapid hypothesis generation in the context of renal pathophysiology.

Published
2012

17. [Kidney and HIV infection]

Author

Plaisier, Emmanuelle, Lescure, François-Xavier, Ronco, Pierre, Remodelage et Reparation du Tissu Renal, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service des maladies infectieuses et tropicales [CHU Tenon], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), RONCO, Pierre, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)

Subjects
MESH: Kidney Diseases, MESH: Adenine, MESH: Humans, urogenital system, MESH: Virus Replication, MESH: Genetic Predisposition to Disease, virus diseases, MESH: Kidney, MESH: Receptor, Epidermal Growth Factor, urologic and male genital diseases, female genital diseases and pregnancy complications, MESH: Male, MESH: HIV-1, MESH: Biopsy, MESH: Glomerular Filtration Rate, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], MESH: African Continental Ancestry Group, MESH: Anti-HIV Agents, MESH: Phosphorus, MESH: AIDS-Associated Nephropathy, MESH: Organophosphonates, MESH: Female
Abstract

International audience; Screening of chronic kidney disease (CKD) that includes estimation of the glomerular filtration rate (GFR) and evaluation proteinuria should be performed in all HIV-infected patients and these parameters have to be monitored annually in patients at higher risk for CKD. Black patients have a genetic predisposition to develop HIV-associated nephropathy. Suppression of HIV viral replication with antiretroviral therapy prevents the development of HIV-associated nephropathy or halts its progression. Kidney biopsy remains the most informative diagnosis test to differentiate various forms of kidney diseases in HIV-infected patients. Dosing antiretroviral agents with kidney metabolism should be adjusted when eGFR is bellow 50 mL/min/1.73 m(2). eGFR and serum phosphorus at baseline and during treatment should be carefully assessed in patients receiving tenofovir. Proximal renal tubular toxicity must be further evaluated in the presence of eGFR decrease and/or hypophosphatemia under tenofovir therapy.

Published
2012

18. The ERA-EDTA Working Group on inherited kidney disorders

Author

Corinne Antignac, Patrick H. Maxwell, Giuseppe Remuzzi, Franz Schaefer, Francesco Emma, Albert C.M. Ong, Dominique Chauveau, Olivier Devuyst, René J. M. Bindels, Pierre Ronco, Ron T. Gansevoort, RONCO, Pierre, Institute of Physiology, Universität Zürich [Zürich] = University of Zurich (UZH)-Zurich Center for Integrative Human Physiology, Klinik für Nephrologie, UniversitätsSpital, Division of Nephrology, UCL Medical School, Néphropathies héréditaires et rein en développement (UMR_S 983), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Department of Physiology, Radboud University Medical Center [Nijmegen], Service de Néphrologie - Immunologie Clinique [Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-PRES Université de Toulouse, Division of Nephrology and Dialysis, IRCCS Ospedale Pediatrico Bambino Gesù [Roma], Department of Nephrology, University Medical Center, University of Groningen, UCL Division of Medicine, University College of London [London] (UCL), Kidney Genetics Group, University of Sheffield Medical School, Mario Negri Institute for Pharmacological Research, CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Division of Pediatric Nephrology, Universität Heidelberg [Heidelberg], Center for Rare Diseases, Universität Heidelberg [Heidelberg]-University Medicine Heidelberg, Cardiovascular Centre (CVC), Groningen Kidney Center (GKC), University of Zurich, Devuyst, Olivier, CHU Toulouse [Toulouse]-Hôpital de Rangueil, CHU Toulouse [Toulouse]-PRES Université de Toulouse, and Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
Pathology, 2747 Transplantation, cystic diseases, medicine.medical_treatment, 030232 urology & nephrology, Physiology, tubulopathies, 10052 Institute of Physiology, MESH: Kidney Transplantation, 0302 clinical medicine, 10035 Clinic for Nephrology, genetics, MESH: Renal Dialysis, 030212 general & internal medicine, Societies, Medical, Cystic disease, 2727 Nephrology, MESH: Genetic Predisposition to Disease, rare diseases, MESH: Nephrology, 3. Good health, Clinical Practice, Europe, Nephrology, 10076 Center for Integrative Human Physiology, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Kidney Diseases, Hemodialysis, medicine.medical_specialty, MESH: Societies, Medical, 610 Medicine & health, patient organization, 03 medical and health sciences, Renal Dialysis, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], medicine, Humans, Genetic Predisposition to Disease, Cystic diseases, Transplantation, MESH: Kidney Diseases, MESH: Humans, business.industry, urogenital system, medicine.disease, Patient organization, Kidney Transplantation, Membrane transport and intracellular motility Renal disorder [NCMLS 5], CLINICAL-PRACTICE, 570 Life sciences, biology, Kidney disorder, MESH: Europe, business, Kidney disease
Abstract

International audience; Dozens of inherited diseases affect the kidney; collectively, they account for at least 10% of patients with end-stage renal disease in Europe [1]. The underlying genetic defects may affect all structures and cell types of the nephron and may therefore compromise all aspects of kidney function. In addition, extra-renal involvement is frequently associated. In terms of frequency, inherited kidney disorders vary from relatively frequent diseases, such as autosomal dominant polycystic kidney disease (ADPKD, that arguably affects one in every 1000 person), to 'rare' diseases that, by definition, affect less than five persons in every 10 000.

Published
2012

19. Timing and determinants of erythropoietin deficiency in chronic kidney disease. : Erythropoietin and chronic kidney disease

Author

Mercadal, Lucile, Metzger, Marie, Casadevall, Nicole, Haymann, Jean-Philippe, Karras, Alexandre, Boffa, Jean-Jacques, Flamant, Martin, Vrtovsnik, François, Stengel, Bénédicte, Froissart, Marc, Centre de recherche en épidémiologie et santé des populations ( CESP ), Université de Versailles Saint-Quentin-en-Yvelines ( UVSQ ) -Université Paris-Sud - Paris 11 ( UP11 ) -Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Service d'hématologie clinique et de thérapie cellulaire [CHU Saint-Antoine], Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Saint-Antoine [APHP], Hématopoïèse normale et pathologique, Université Paris-Sud - Paris 11 ( UP11 ) -Institut Gustave Roussy ( IGR ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Remodelage et Reparation du Tissu Renal, Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Service de Physiologie [Tenon], Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Tenon [APHP], Service de Néphrologie [HEGP], Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Européen Georges Pompidou [APHP] ( HEGP ), Service de Néphrologie et Dialyses [CHU Tenon], Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Tenon [APHP], Service de Physiologie [Bichat-Claude Bernard], Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Assistance publique - Hôpitaux de Paris (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Immunopathologie rénale, récepteurs et inflammation, Université Paris Diderot - Paris 7 ( UPD7 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Service de Néphrologie [Bichat-Claude Bernard], Service de physiologie, explorations fonctionnelles et radioisotopes [CHU HEGP], Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Européen Georges Pompidou [APHP] ( HEGP ), The NephroTest CKD cohort study is supported by grants from: Inserm GIS-IReSP AO - 8113LS TGIR (BS), French Ministry of Health AOM 09114 (MF), Inserm AO 8022LS (BS), Agence de la Biomédecine R0 8156LL (BS), AURA (MF) and Roche 2009-152-447G (MF). The Nephrotest initiative was also sponsored by unrestricted grants from F.Hoffman-La Roche Ltd. (LM)., Nephrotest Study Group, Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Tenon [AP-HP], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Gustave Roussy (IGR)-Université Paris-Sud - Paris 11 (UP11), Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Tenon [AP-HP], and Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)

Subjects
MESH : Male, MESH : Aged, MESH : Hemoglobins, MESH: Multivariate Analysis, MESH : Chronic Disease, hemic and lymphatic diseases, MESH : Erythropoietin, MESH : Middle Aged, MESH : Female, MESH: Erythropoietin, MESH: Aged, MESH: Kidney Diseases, MESH: Middle Aged, MESH: Humans, MESH: Chronic Disease, MESH: Time Factors, MESH : Humans, MESH : Glomerular Filtration Rate, MESH : Multivariate Analysis, MESH: Adult, [ SDV.SPEE ] Life Sciences [q-bio]/Santé publique et épidémiologie, MESH : Adult, MESH: Male, MESH: Glomerular Filtration Rate, MESH: Hemoglobins, MESH : Kidney Diseases, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, MESH: Female, MESH : Time Factors
Abstract

International audience; BACKGROUND AND OBJECTIVES: Anemia in patients with CKD is highly related to impaired erythropoietin (EPO) response, the timing and determinants of which remain unknown. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This study measured EPO levels and studied their relation to GFR measured by 51Cr-EDTA renal clearance (mGFR) in 336 all-stage CKD patients not receiving any erythropoiesis-stimulating agent. RESULTS: In patients with anemia defined by World Health Organization criteria (hemoglobin [Hb] 30 ml/min per 1.73 m(2), whereas they were not correlated when mGFR was 30 ml/min per 1.73 m(2) calls for other explanatory factors.

Published
2012

20. Timing and determinants of erythropoietin deficiency in chronic kidney disease

Author

Mercadal, Lucile, Metzger, Marie, Casadevall, Nicole, Haymann, Jean-Philippe, Karras, Alexandre, Boffa, Jean-Jacques, Flamant, Martin, Vrtovsnik, François, Stengel, Bénédicte, Froissart, Marc, De Lauzon-Guillain, Blandine, Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'hématologie clinique et de thérapie cellulaire [CHU Saint-Antoine], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Hématopoïèse normale et pathologique, Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Remodelage et Reparation du Tissu Renal, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service de Néphrologie [HEGP], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Service de Département de Néphrologie = Service de Néphrologie et Dialyses [CHU Tenon], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service de Physiologie [Bichat-Claude Bernard], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Immunopathologie rénale, récepteurs et inflammation, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Néphrologie [Bichat-Claude Bernard], Service de physiologie, explorations fonctionnelles et radioisotopes [CHU HEGP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), The NephroTest CKD cohort study is supported by grants from: Inserm GIS-IReSP AO - 8113LS TGIR (BS), French Ministry of Health AOM 09114 (MF), Inserm AO 8022LS (BS), Agence de la Biomédecine R0 8156LL (BS), AURA (MF) and Roche 2009-152-447G (MF). The Nephrotest initiative was also sponsored by unrestricted grants from F.Hoffman-La Roche Ltd. (LM)., and Nephrotest Study Group

Subjects
MESH: Aged, MESH: Kidney Diseases, MESH: Middle Aged, MESH: Humans, MESH: Chronic Disease, MESH: Time Factors, MESH: Adult, MESH: Multivariate Analysis, MESH: Male, MESH: Glomerular Filtration Rate, MESH: Hemoglobins, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, hemic and lymphatic diseases, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, MESH: Erythropoietin, MESH: Female
Abstract

International audience; BACKGROUND AND OBJECTIVES: Anemia in patients with CKD is highly related to impaired erythropoietin (EPO) response, the timing and determinants of which remain unknown. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This study measured EPO levels and studied their relation to GFR measured by 51Cr-EDTA renal clearance (mGFR) in 336 all-stage CKD patients not receiving any erythropoiesis-stimulating agent. RESULTS: In patients with anemia defined by World Health Organization criteria (hemoglobin [Hb] 30 ml/min per 1.73 m(2), whereas they were not correlated when mGFR was 30 ml/min per 1.73 m(2) calls for other explanatory factors.

Published
2012

21. Thrombospondin-1 plays a profibrotic and pro-inflammatory role during ureteric obstruction

Author

Sophie Vandermeersch, Naïke Bigé, Pierre Ronco, Safa Benhassine, Christos Chatziantoniou, Chantal Jouanneau, Jean-Jacques Boffa, Jean-Claude Dussaule, Nasim Shweke, RONCO, Pierre, CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Remodelage et Reparation du Tissu Renal, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Saint-Antoine [AP-HP], Institut National de la Santé et de la Recherche Médicale and Université Pierre et Marie Curie., and Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
Male, Vascular Endothelial Growth Factor A, MESH: Signal Transduction, Time Factors, Apoptosis, MESH: Rats, Sprague-Dawley, Kidney, urologic and male genital diseases, Peritubular capillaries, Nephrectomy, MESH: Mice, Knockout, Rats, Sprague-Dawley, Thrombospondin 1, Mice, MESH: Transforming Growth Factor beta1, 0302 clinical medicine, Fibrosis, MESH: Animals, Renal stem cell, Chemokine CCL2, MESH: Thrombospondin 1, Mice, Knockout, MESH: Collagen Type III, 0303 health sciences, Nephritis, renal progression, renal fibrosis, MESH: Gene Expression Regulation, 3. Good health, medicine.anatomical_structure, Nephrology, 030220 oncology & carcinogenesis, MESH: Fibrosis, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Kidney Diseases, medicine.symptom, Inflammation Mediators, MESH: Nephritis, Signal Transduction, Ureteral Obstruction, TGF-β, medicine.medical_specialty, MESH: Rats, MESH: Inflammation Mediators, Inflammation, MESH: Atrophy, Transforming Growth Factor beta1, 03 medical and health sciences, Internal medicine, MESH: Cell Proliferation, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], medicine, Renal fibrosis, Animals, MESH: Mice, MESH: Chemokine CCL2, 030304 developmental biology, Cell Proliferation, MESH: Capillaries, MESH: Kidney Diseases, business.industry, MESH: Apoptosis, MESH: Vascular Endothelial Growth Factor A, MESH: Chronic Disease, MESH: Time Factors, Kidney metabolism, MESH: Kidney, medicine.disease, MESH: Male, Capillaries, Rats, MESH: Nephrectomy, Disease Models, Animal, Endocrinology, Collagen Type III, Gene Expression Regulation, Chronic Disease, Atrophy, MESH: Ureteral Obstruction, MESH: Disease Models, Animal, business, Kidney disease, Transforming growth factor
Abstract

International audience; Thrombospondin-1 (TSP-1) is an endogenous activator of transforming growth factor-β (TGF-β), and an anti-angiogenic factor, which may prevent kidney repair. Here we investigated whether TSP-1 is involved in the development of chronic kidney disease using rats with unilateral ureteral obstruction, a well-known model to study renal fibrosis. Obstruction of 10 days duration induced inflammation, tubular cell atrophy, dilation, apoptosis, and proliferation, leading to interstitial fibrosis. TSP-1 expression was increased in parallel to that of collagen III and TGF-β. Relief of the obstruction at day 10 produced a gradual improvement in renal structure and function, the reappearance of peritubular capillaries, and restoration of renal VEGF content over a 7- to 15-day post-relief period. TSP-1 expression decreased in parallel with that of TGF-β1 and collagen III. Mice in which the TSP-1 gene was knocked out displayed less inflammation and had better preservation of renal tissue and the peritubular capillary network compared to wild-type mice. Additional studies showed that the inflammatory effect of TSP-1 was mediated, at least in part, by monocyte chemoattractant protein-1 and activation of the Th17 pathway. Thus, TSP-1 is an important profibrotic and inflammatory mediator of renal disease. Blockade of its action may be a treatment against the development of chronic kidney disease.

Published
2012

22. [Renal disorders associated with monoclonal gammopathies: diagnostic and therapeutic progress]

Author

Bridoux, Franck, Delbes, Sébastien, Sirac, Christophe, Pourreau, François, Puyade, Matthieu, Desport, Estelle, Jaccard, Arnaud, Fermand, Jean-Paul, Touchard, Guy, Contrôle de la Réponse Immune B et des Lymphoproliférations (CRIBL), Centre National de la Recherche Scientifique (CNRS)-Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503), Service de néphrologie - hémodialyse et transplantation rénale, Centre hospitalier universitaire de Poitiers (CHU Poitiers), Service d'hématologie clinique et de thérapie cellulaire [CHU Saint-Antoine], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Centre National de la Recherche Scientifique (CNRS), and Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Saint-Antoine [APHP]

Subjects
MESH: Immunoglobulin Light Chains, Biopsy, Paraproteinemias, Kidney, Dexamethasone, MESH: Kidney Transplantation, Bortezomib, MESH: Biopsy, MESH: Melphalan, MESH: Paraproteinemias, Humans, MESH: Amyloidosis, Melphalan, MESH: Kidney Diseases, MESH: Humans, Plasma Exchange, MESH: Heart Transplantation, MESH: Kidney, Amyloidosis, MESH: Plasma Exchange, Boronic Acids, Kidney Transplantation, MESH: Pyrazines, MESH: Dexamethasone, Pyrazines, [SDV.IMM]Life Sciences [q-bio]/Immunology, Heart Transplantation, MESH: Boronic Acids, Immunoglobulin Light Chains, Kidney Diseases, Immunoglobulin Heavy Chains, MESH: Immunoglobulin Heavy Chains
Abstract

International audience; Various renal disorders are associated with monoclonal gammopathies, secondary to tissue deposition or precipitation of a monoclonal immunoglobulin (Ig) or a fragment thereof (isolated Ig light chain or heavy chain). They are classified according to the localization of renal lesions, either glomerular or tubular and to the pattern of ultrastructural organization of Ig deposits. Renal disease in monoclonal gammopathies may be isolated, or associated with various systemic symptoms particularly in AL amyloidosis, Randall-type monoclonal Ig deposition disease and monoclonal cryoglobulinemias. Except for myeloma cast nephropathy, which occurs in the setting of high-mass myeloma and is recognized after electrophoretic analysis of proteinuria and AL amyloidosis, which diagnosis is usually made after pathological examination of non-invasive tissue specimens (i.e. abdominal fat or minor salivary glands), a kidney biopsy is required to identify the other types of renal disorders associated with monoclonal gammopathies and to estimate renal prognosis. Renal pathological diagnosis is difficult and relies on careful examination of kidney biopsy samples, by light microscopy, immunofluorescence studies using conjugates specific for Ig light and heavy chains, IgG sub-classes and heavy chain constant domains and by electron microscopy. In some cases, additional studies are required to identify the nature of deposits, such as immuno-electron microscopy or mass spectrometric-based proteomic analysis after laser dissection. In patients with renal disorders related to Ig light chain precipitation or deposition (myeloma cast nephropathy, AL amyloidosis, Randall-type light chain deposition disease), measurement of serum free light chains at baseline and throughout follow-up is mandatory to evaluate clonal response to chemotherapy. A more than or equal to 50% decrease in serum free light chain levels is associated with increased renal and patient survival. In AL amyloidosis, serum levels of markers of cardiac disease (NT-proBNP and troponin) are also closely associated with prognosis. Efficient chemotherapy, tailored to the underlying plasma cell or lymphoproliferative disorder and adapted to renal function, should be promptly introduced, even in the absence of overt malignant haematological disease. Renal prognosis and patient survival (particularly in AL amyloidosis and cast nephropathy) are closely associated with the rapid achievement of an haematological response. The combination of melphalan plus dexamethasone (MDex) is currently used as first-line chemotherapy in systemic AL amyloidosis. Bortezomib-based regimens are commonly employed as first-line treatment in myeloma cast nephropathy and Randall-type monoclonal Ig deposition disease and as second line therapy in AL amyloidosis patients with advanced cardiomyopathy or refractory to previous chemotherapy. Solid organ transplantation (heart and kidney) should be considered in patients with AL amyloidosis or Randall-type monoclonal Ig deposition disease and advanced cardiac or renal failure. Prolonged graft and patient survival may be obtained, providing that recipients do not have other severe organ involvement or symptomatic myeloma and that haematological remission has been achieved with chemotherapy before or after organ transplantation.

Published
2011

23. [Kidney diseases: new issues]

Author

Ronco, Pierre, Remodelage et Reparation du Tissu Renal, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), and RONCO, Pierre

Subjects
MESH: Kidney Diseases, MESH: Humans, MESH: Chronic Disease, MESH: Renal Insufficiency, Chronic, MESH: Biological Markers, MESH: Cardiovascular Diseases, urologic and male genital diseases, Prognosis, female genital diseases and pregnancy complications, MESH: Prognosis, MESH: France, Cohort Studies, Cardiovascular Diseases, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Chronic Disease, Disease Progression, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Humans, MESH: Disease Progression, Kidney Diseases, France, Renal Insufficiency, Chronic, MESH: Cohort Studies, Biomarkers
Abstract

International audience; Chronic kidney disease (CKD) affects two to four million people in France and most of them are not aware of their disease. CKD is a major, independent risk factor of cardiovascular mortality and morbidity; the cardiovascular risk increases with the severity of renal failure. Evaluation of renal function (GFR) relies on MDRD and CKD-EPI equations. The French CKD-REIN cohort with more than 3000 patients followed for 5 years, will hopefully provide substantial advances in the knowledge of CKD epidemiology, of risk factors and mechanisms of CKD progression and medical practices. Improving CKD screening based on blood pressure, proteinuria (microalbuminuria in diabetic patients) and serum creatinine, is a national duty in high risk patients (with diabetes, hypertension and cardiovascular diseases). A major research goal is to identify new therapeutic targets and biomarkers, in order to treat kidney diseases before the occurrence of renal insufficiency, to halt their progression and to decrease cardiovascular risk. Careful therapeutic education of patients is required to successfully implement established guidelines, appropriate diets and new therapeutic strategies.

Published
2011

24. Renal transplantation in patients with AA amyloidosis nephropathy: results from a French multicenter study

Author

P. Le Pogamp, Nicolas Bouvier, Julien Zuber, Vincent Audard, Tomek Kofman, Julie Peltier, Laetitia Albano, Lionel Couzi, P. Lang, Claire Pouteil-Noble, Luc Frimat, A. Le Thuaut, Gabriel Choukroun, Nassim Kamar, Florence Canoui-Poitrine, Mathias Büchler, G. Couvrat, Christiane Mousson, Valérie Garrigue, Philippe Grimbert, Franck Bridoux, Michel Delahousse, Christophe Mariat, Evangeline Pillebout, Contrôle de la Réponse Immune B et des Lymphoproliférations (CRIBL), Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Centre National de la Recherche Scientifique (CNRS), Service de néphrologie - hémodialyse et transplantation rénale, and Centre hospitalier universitaire de Poitiers (CHU Poitiers)

Subjects
Male, 030232 urology & nephrology, Kaplan-Meier Estimate, 030204 cardiovascular system & hematology, Gastroenterology, MESH: Kidney Transplantation, 0302 clinical medicine, AA amyloidosis, Recurrence, Immunology and Allergy, Pharmacology (medical), Kidney transplantation, MESH: Treatment Outcome, Kidney, MESH: Middle Aged, Amyloidosis, Graft Survival, Middle Aged, 3. Good health, Treatment Outcome, medicine.anatomical_structure, Cardiovascular Diseases, MESH: Kidney Failure, Chronic, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Kidney Diseases, MESH: Infection, Adult, medicine.medical_specialty, MESH: Graft Survival, Urinary system, Infections, Nephropathy, 03 medical and health sciences, Internal medicine, medicine, Humans, MESH: Amyloidosis, MESH: Kaplan-Meier Estimate, Retrospective Studies, Transplantation, MESH: Kidney Diseases, MESH: Humans, business.industry, MESH: Cardiovascular Diseases, MESH: Adult, MESH: Retrospective Studies, medicine.disease, Kidney Transplantation, MESH: Male, Surgery, MESH: Recurrence, Kidney Failure, Chronic, business, MESH: Female, Kidney disease
Abstract

International audience; Although end-stage renal disease related to AA amyloidosis nephropathy is well characterized, there are limited data concerning patient and graft outcome after renal transplantation. We performed a multicentric retrospective survey to assess the graft and patient survival in 59 renal recipients with AA amyloidosis. The recurrence rate of AA amyloidosis nephropathy was estimated at 14%. The overall, 5- and 10-year patient survival was significantly lower for the AA amyloidosis patients than for a control group of 177 renal transplant recipients (p = 0.0001, 0.028 and 0.013, respectively). In contrast, we did not observe any statistical differences in the 5- and 10- year graft survival censored for death between two groups. AA amyloidosis-transplanted patients exhibited a high proportion of infectious complications after transplantation (73.2%). Causes of death included both acute cardiovascular events and fatal septic complications. Multivariate analysis demonstrated that the recurrence of AA amyloidosis on the graft (adjusted OR = 14.4, p = 0.01) and older recipient age (adjusted OR for a 1-year increase = 1.06, p = 0.03) were significantly associated with risk of death. Finally, patients with AA amyloidosis nephropathy are eligible for renal transplantation but require careful management of both cardiovascular and infectious complications to reduce the high risk of mortality.

Published
2011

25. [Renal biopsy practice: results of a French study and recommendations]

Author

Bollée , Guillaume, Moulin , Bruno, Martinez , Frank, Meulders , Quentin, Rougier , Jean-Philippe, Baumelou , Alain, Glotz , Denis, Subra , Jean-François, Ulinski , Tim, Vrigneaud , Laurence, Brasseur , José, Alhenc-Gelas , Martine, Martin , Laurent, DANIEL , Laurent, Kourilsky , Olivier, Deteix , Patrice, Sie , Pierre, Ronco , Pierre, Houillier , Pascal, Laboratoire de Recherche en Imagerie : Méthodes d'imagerie des Échanges transcapillaires (LRI - EA4062), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Néphrologie et Transplantation, CHU Strasbourg, Service de Transplantation Rénale, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Descartes - Paris 5 (UPD5)-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service de Néphrologie [Avignon], Centre Hospitalier Henri Duffaut (Avignon), CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), CHU Pitié-Salpêtrière [AP-HP], Service de Néphrologie [Saint-Louis], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Service de Néphrologie [Angers], Université d'Angers (UA)-Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM), CHU Trousseau [APHP], Service de Néphrologie [Valenciennes], Centre Hospitalier de Valenciennes, Service de Néphrologie [Bois-Bernard], Hôpital privé Bois-Bernard, Service d'Hématologie [Georges-Pompidou], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Université Paris Descartes - Paris 5 (UPD5), Service de Pathologie [CHU de Dijon], Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Laboratoire d'Anatomopathologie [Aix-Marseille], Assistance Publique - Hôpitaux de Marseille (APHM)- Hôpital de la Timone [CHU - APHM] (TIMONE), Service de Néphrologie [Evry], Centre Hospitalier Sud Francilien, Service de Néphrologie [Clermont-Ferrand], CHU Clermont-Ferrand-Université d'Auvergne - Clermont-Ferrand I (UdA), Service Hématologie - IUCT-Oncopole [CHU Toulouse], Pôle Biologie [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Pôle IUCT [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Service de Physiologie [Georges-Pompidou], Service de Néphrologie et Dialyses [CHU Tenon], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service de Néphrologie [CHU Pitié-Salpêtrière], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), CH Evry-Corbeil-CH Evry-Corbeil, Laboratoire d'Hématologie [Rangueil], Hôpital de Rangueil, CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse], RONCO, Pierre, Service de Département de Néphrologie = Service de Néphrologie et Dialyses [CHU Tenon], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service de néphrologie [CHU Pitié-Salpêtrière], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Laboratoire de Recherche en Imagerie : Méthodes d'imagerie des Échanges transcapillaires ( LRI - EA4062 ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Paris Descartes - Paris 5 ( UPD5 ), Assistance publique - Hôpitaux de Paris (AP-HP)-Université Paris Descartes - Paris 5 ( UPD5 ) -CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Tenon [APHP], Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Pitié-Salpêtrière [APHP], Assistance publique - Hôpitaux de Paris (AP-HP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Université d'Angers ( UA ) -CHU Angers, Service de Néphrologie Pédiatrique [Trousseau], Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Européen Georges Pompidou [APHP] ( HEGP ) -Université Paris Descartes - Paris 5 ( UPD5 ), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand ( CHU Dijon ), Assistance Publique - Hôpitaux de Marseille ( APHM ) - Hôpital de la Timone [CHU - APHM] ( TIMONE ), CHU Clermont-Ferrand-Université d'Auvergne - Clermont-Ferrand I ( UdA ), Université Toulouse III - Paul Sabatier ( UPS ), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Hôpital de Rangueil, and CHU Toulouse [Toulouse]

Subjects
MESH: Kidney Diseases, MESH: Humans, Biopsy, MESH : Humans, MESH: Kidney, Kidney, MESH : Kidney, MESH: France, MESH: Biopsy, MESH : Physician's Practice Patterns, [ SDV.BBM.GTP ] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], MESH : Biopsy, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], MESH : Kidney Diseases, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Humans, Kidney Diseases, France, Practice Patterns, Physicians', MESH : France, MESH: Physician's Practice Patterns
Abstract

International audience; BACKGROUND: Although several risk factors associated with complications after renal biopsy (RB) have been identified, recommendations for RB procedures are still lacking. Our working group, appointed by the scientific commission of the Société de néphrologie in France, aimed to depict the main aspects of the practice of RB in adults in France, before establishing some guidelines. METHODS: Members of the Société de néphrologie in France were asked to participate to a questionnaire survey on RB procedures. RESULTS: Eighty-eight nephrologists from 74 units (27 in teaching hospitals, 35 in public general hospitals, and 12 in private centers) participated in our study. Native kidney and graft biopsies were performed in 73 and 35 units, respectively. RB activity was highly variable among units, ranging from several hundred to less than ten per year. Transjugular RB was judged to be smoothly accessible in 28 out of 73 units (38.4%). Significant variations in practices were observed regarding patient information before RB, assessment of hemorrhagic risk factors, care of patients with antiplatelet agents and hemorrhagic risk factors, and radiological guidance. Early discharge (

Published
2011

26. Renal tubular fluid shear stress promotes endothelial cell activation

Author

Christiane Pecher, Mathieu Miravète, Muriel Mercier-Bonin, Julie Klein, Joost P. Schanstra, Bénédicte Buffin-Meyer, Aurèle Besse-Patin, Jean-Loup Bascands, Julien Gonzalez, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'Ingénierie des Systèmes Biologiques et des Procédés (LISBP), Centre National de la Recherche Scientifique (CNRS)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de la Recherche Agronomique (INRA), Institut National de la Recherche Agronomique (INRA)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS), Simon, Marie Francoise, and Institut National des Sciences Appliquées (INSA)-Université Fédérale Toulouse Midi-Pyrénées-Institut National des Sciences Appliquées (INSA)-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)

Subjects
MESH: Inflammation, Chemokine, Tubular fluid, 030232 urology & nephrology, Urine, MESH: Monocytes, Biochemistry, Monocytes, MESH: Urine, 0302 clinical medicine, MESH: Endothelial Cells, Chemokine CCL2, 0303 health sciences, Kidney, MESH: Stress, Mechanical, biology, MESH: Culture Media, Conditioned, Endothelial stem cell, medicine.anatomical_structure, Kidney Tubules, MESH: Kidney Tubules, Tumor necrosis factor alpha, Kidney Diseases, MESH: Shear Strength, medicine.symptom, Shear Strength, medicine.medical_specialty, Biophysics, Vascular Cell Adhesion Molecule-1, Inflammation, CCL2, MESH: Cell Adhesion, 03 medical and health sciences, Internal medicine, medicine, Cell Adhesion, Humans, Autocrine signalling, Molecular Biology, MESH: Chemokine CCL2, 030304 developmental biology, MESH: Kidney Diseases, MESH: Humans, Tumor Necrosis Factor-alpha, MESH: Vascular Cell Adhesion Molecule-1, Endothelial Cells, Cell Biology, Endocrinology, Culture Media, Conditioned, MESH: Tumor Necrosis Factor-alpha, Immunology, biology.protein, Stress, Mechanical
Abstract

International audience; Modified urinary fluid shear stress (FSS) induced by variations of urinary fluid flow and composition is observed in early phases of most kidney diseases. In this study, we hypothesized that changes in urinary FSS represent a tubular aggression that contributes to the development of inflammation, a key event in progression of nephropathies. Human renal tubular cells (HK-2) were exposed to FSS for 30 min at 0.01 Pa. Treatment of human endothelial cells (HMEC-1) with the resulting conditioned medium (FSS-CM) increased C-C chemokine ligand 2 (CCL2) and tumor necrosis factor (TNF)-α protein secretion, increased endothelial vascular adhesion molecule-1 (VCAM-1) mRNA expression and stimulated adhesion of human (THP-1) monocytes to the endothelial monolayer. These effects were TNF-α dependent as they were abolished by neutralization of TNF-α. Interestingly, the origin of TNF-α was not epithelial, but resulted from autocrine endothelial production. However, in contrast to short term FSS, long term FSS (5h) induced the release of the key inflammatory proteins CCL2 and TNF-α directly from tubular cells. In conclusion, these results suggest for the first time that urinary FSS can contribute to the inflammatory state involved in initiation/perpetuation of renal diseases.

Published
2011

27. Identification of tubular heparan sulfate as a docking platform for the alternative complement component properdin in proteinuric renal disease

Author

Romain R. Vivès, Harry van Goor, Jacob van den Born, Pieter van der Pol, Marc A. Seelen, Azadeh Zaferani, Jelleke J. Hakvoort, Mohamed R. Daha, Gerjan Navis, Hugues Lortat-Jacob, Institut de biologie structurale (IBS - UMR 5075 ), Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Groningen Institute for Organ Transplantation (GIOT), Groningen Kidney Center (GKC), Lifestyle Medicine (LM), Vascular Ageing Programme (VAP), Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), and Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)

Subjects
Male, Complement Pathway, Alternative, 030232 urology & nephrology, Glycobiology and Extracellular Matrices, urologic and male genital diseases, Biochemistry, Kidney Tubules, Proximal, chemistry.chemical_compound, 0302 clinical medicine, Sulfation, BINDING, PROXIMAL TUBULES, MESH: Animals, TUBULOINTERSTITIAL INJURY, PROTEOGLYCANS, DAMAGE, 0303 health sciences, Kidney, PATHWAY ACTIVATION, MESH: Immunologic Factors, MESH: Complement C3, Complement C3, Heparin, Heparan sulfate, female genital diseases and pregnancy complications, Cell biology, Proteinuria, medicine.anatomical_structure, MESH: Epithelial Cells, Kidney Diseases, Protein Binding, medicine.drug, MESH: Rats, chemical and pharmacologic phenomena, 03 medical and health sciences, KIDNEY, MESH: Proteinuria, MESH: Heparitin Sulfate, MESH: Kidney Tubules, Proximal, medicine, BRUSH-BORDER, Animals, Humans, Immunologic Factors, MESH: Protein Binding, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Rats, Wistar, Molecular Biology, 030304 developmental biology, GLYCOSAMINOGLYCANS, MESH: Kidney Diseases, MESH: Humans, Properdin, MESH: Heparin Lyase, Epithelial Cells, Cell Biology, MESH: Rats, Wistar, Heparin lyase, MESH: Male, Rats, Complement system, Heparin Lyase, chemistry, CELLS, Alternative complement pathway, Heparitin Sulfate, MESH: Properdin, MESH: Complement Pathway, Alternative
Abstract

International audience; Properdin binds to proximal tubular epithelial cells (PTEC) and activates the complement system via the alternative pathway in vitro. Cellular ligands for properdin in the kidney have not yet been identified. Because properdin interacts with solid-phase heparin, we investigated whether heparan sulfate proteoglycans (HSPG) could be the physiological ligands of properdin. Kidneys from proteinuric rats showed colocalization of syndecan-1, a major epithelial HSPG, and properdin in the apical membranes of PTEC, which was not seen in control renal tissue. In vitro, PTEC did not constitutively express properdin. However, exogenous properdin binds to these cells in a dose-dependent fashion. Properdin binding was prevented by heparitinase pretreatment of the cells and was dose-dependently inhibited by exogenous heparin. ELISA and surface plasmon resonance spectroscopy (BIAcore) showed a strong dose-dependent interaction between heparan sulfate (HS) and properdin (K(d) = 128 nm). Pretreatment of HSPG with heparitinase abolished this interaction in ELISA. Competition assays, using a library of HS-like polysaccharides, showed that sulfation pattern, chain length, and backbone composition determine the interaction of properdin with glycosaminoglycans. Interestingly, two nonanticoagulant heparin derivatives inhibited properdin-HS interaction in ELISA and BIAcore. Incubation of PTEC with human serum as complement source led to complement activation and deposition of C3 on the cells. This C3 deposition is dependent on the binding of properdin to HS as shown by heparitinase pretreatment of the cells. Our data identify tubular HS as a novel docking platform for alternative pathway activation via properdin, which might play a role in proteinuric renal damage. Our study also suggests nonanticoagulant heparinoids may provide renoprotection in complement-dependent renal diseases.

Published
2011

28. Warm ischaemia: the ultimate enemy for partial nephrectomy?

Author

Fabien Bouliere, Jean-Jacques Patard, Géraldine Pignot, Service d'urologie [CHU Cochin], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service d'urologie, Hôpital Bicêtre-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11), Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Bicêtre, De Villemeur, Hervé, Assistance publique - Hôpitaux de Paris (AP-HP) - CHU Cochin [AP-HP], and Université Paris-Sud - Paris 11 (UP11) - Assistance publique - Hôpitaux de Paris (AP-HP) - Hôpital Bicêtre

Subjects
medicine.medical_specialty, [SDV.MHEP.CHI] Life Sciences [q-bio]/Human health and pathology/Surgery, Urology, medicine.medical_treatment, Population, 030232 urology & nephrology, Ischemia, Renal function, [SDV.MHEP.CHI]Life Sciences [q-bio]/Human health and pathology/Surgery, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, New onset, 03 medical and health sciences, Impaired renal function, 0302 clinical medicine, medicine, MESH: Warm Ischemia, Risk factor, education, ComputingMilieux_MISCELLANEOUS, education.field_of_study, MESH: Kidney Diseases, MESH: Humans, business.industry, MESH: Time Factors, medicine.disease, [SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, Nephrectomy, 3. Good health, MESH: Nephrectomy, 030220 oncology & carcinogenesis, MESH: Kidney Neoplasms, business, Kidney disease
Abstract

Partial nephrectomy (PN) has gained popularity due to the increased incidenceof small incidental renal tumoursandthe procedure’s excellent oncologic results; however, current scientific evidence suggests that preservation of renal function should be given priority. Go and al [1] showed an independent, gradedassociation between reduced estimated glomerular filtration rate (GFR) and the risks of cardiovascular events, hospitalisation, and death from any cause in a large community-based population. Radical nephrectomy is now understood as a risk factor for chronic kidney disease, which in turn increases the risk of cardiovascular events and all-cause mortality. Huang et al [2] demonstrated in 662 patient-candidates for radical nephrectomy or PN that 26% had a certain degree of impaired renal function at baseline. This study also highlighted that the risk of new onset of chronickidneydiseasewas significantly increased inpatients undergoing radical nephrectomy versus PN. Four recent series have confirmed that patients treated with radical nephrectomy are at increased risk of non–cancer-related death when compared with those being treated with PN. Specifically, Weight et al [3] demonstrated that in patients with T1b tumours, the average excess loss of renal function observed with radical nephrectomy was associated with a 25% increased riskof cardiacdeathanda17% increased riskof death from any cause. These accumulated data should prompt us to choose options that are less deleterious to renal function when determining treatment for small renal tumours. It is obvious thata certainnumberof small renal tumoursare indolentand not life threatening; therefore, we should integrate information such as age, comorbidities, baseline renal function

Published
2010

29. Renal biopsies after 70 years of age: a retrospective longitudinal study from 2000 to 2007 on 150 patients in Western France

Author

Cécile Vigneau, Patrick Le Pogamp, Thierry Frouget, Emilie Pinçon, Nathalie Rioux-Leclercq, De Villemeur, Hervé, Service de néphrologie [Rennes], Université de Rennes (UR)-Hôpital Pontchaillou-CHU Pontchaillou [Rennes], Service d'anatomie et cytologie pathologiques [Rennes] = Anatomy and Cytopathology [Rennes], CHU Pontchaillou [Rennes], Institut de Génétique et Développement de Rennes (IGDR), Université de Rennes (UR)-Centre National de la Recherche Scientifique (CNRS), CHU Pontchaillou [Rennes]-Hôpital Pontchaillou-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), Université de Rennes 1 (UR1), and Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, Aging, Health (social science), Biopsy, 030232 urology & nephrology, 030204 cardiovascular system & hematology, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, MESH: Biopsy, 0302 clinical medicine, Elderly, therapeutics, Medicine, Longitudinal Studies, MESH: Longitudinal Studies, MESH: Aged, Kidney, MESH: Statistics, Nonparametric, medicine.diagnostic_test, Mortality rate, 3. Good health, Survival Rate, medicine.anatomical_structure, Female, Kidney Diseases, Renal biopsy, France, medicine.medical_specialty, MESH: Survival Rate, Statistics, Nonparametric, MESH: Prognosis, Nephropathy, 03 medical and health sciences, renal biopsy, Internal medicine, Humans, Survival rate, Aged, Retrospective Studies, MESH: Kidney Diseases, MESH: Humans, business.industry, Retrospective cohort study, MESH: Retrospective Studies, medicine.disease, [SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, MESH: Male, Surgery, MESH: France, prognosis, Geriatrics and Gerontology, business, Gerontology, Nephrotic syndrome, MESH: Female
Abstract

International audience; The elderly are more often referred to nephrologists and questions about indications for renal biopsy are increasing. The vascular lesions that appear with aging make the diagnosis of additional nephropathy more difficult. The purpose of our study is to investigate the characteristics of renal biopsies in the elderly in order to evaluate the indications and their use in guiding specific therapeutic interventions. Patients over 70 years who underwent a renal biopsy between 2000 and 2007 in Rennes University Hospital were retrospectively analyzed for biopsy complications, clinical features, diagnosis, therapy and its complications, evolution and mortality. Among the 150 renal-biopsied patients, 60% had a glomerulopathy and 30% had nephrotic syndrome. Biopsy complications occurred in 3.3%. 64% of nephrotic patients received immunosuppressive treatment and 62% of them developed drug-associated complications. In the treated group, there was more remission and survival at day 1000 was improved. Renal biopsy may be indicated in the elderly, because it often gives a therapeutically useful diagnosis and complications are rare if contra-indications are respected. Kidney biopsy revealed histological diagnoses that were not usually suspected by the clinical presentation. In addition, immunosuppressive therapy did not alter the mortality rate, but did increase survival at 3 years.

Published
2010

30. Chronic kidney disease and cancer: a troubling connection

Author

Stengel, Bénédicte, De Lauzon-Guillain, Blandine, Recherche en épidémiologie et biostatistique, and Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
glomerular filtration rate, MESH: Kidney Diseases, MESH: Humans, spatial analysis, Epidemiology, MESH: Chronic Disease, MESH: Kidney Transplantation, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, MESH: Risk Factors, incidence, MESH: Neoplasms, MESH: Renal Dialysis, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, ESRD
Abstract

International audience; Chronic kidney disease (CKD) and cancer are connected in a number of ways in both directions: cancer can cause CKD either directly or indirectly through the adverse effects of therapies; CKD may, conversely, be a risk factor for cancer; and both may be associated because they share common risk factors, often toxins. In this review, we briefly address the issue of paraneoplastic nephropathies as well as that of toxin-related cancers and CKD, including analgesic and aristolochic acid nephropathies. We then focus on the links between the various stages of CKD and cancer incidence, and critically examine major epidemiologic surveys in the field. Compared with the general population, kidney transplant recipients have a threefold to fourfold increase in overall cancer risk, and relative risks higher than 3 for about 20 specific tumors, most, but not all, of which are known or suspected to be caused by viral agents. After dialysis, cancer risk increases 10% to 80% according to studies, with relative risks significantly higher than in the general population, for about 10 cancer sites. There is emerging evidence for an excess risk of cancer in patients in early CKD stages.

Published
2010

31. Chronic kidney disease and cancer: a troubling connection.: CKD and cancer

Author

Benedicte Stengel, Recherche en épidémiologie et biostatistique, and Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
glomerular filtration rate, MESH: Kidney Diseases, MESH: Humans, spatial analysis, Epidemiology, MESH: Chronic Disease, Kidney Transplantation, Article, MESH: Kidney Transplantation, Renal Dialysis, Risk Factors, MESH: Risk Factors, Neoplasms, Chronic Disease, incidence, Humans, Kidney Diseases, MESH: Neoplasms, MESH: Renal Dialysis, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, ESRD
Abstract

International audience; Chronic kidney disease (CKD) and cancer are connected in a number of ways in both directions: cancer can cause CKD either directly or indirectly through the adverse effects of therapies; CKD may, conversely, be a risk factor for cancer; and both may be associated because they share common risk factors, often toxins. In this review, we briefly address the issue of paraneoplastic nephropathies as well as that of toxin-related cancers and CKD, including analgesic and aristolochic acid nephropathies. We then focus on the links between the various stages of CKD and cancer incidence, and critically examine major epidemiologic surveys in the field. Compared with the general population, kidney transplant recipients have a threefold to fourfold increase in overall cancer risk, and relative risks higher than 3 for about 20 specific tumors, most, but not all, of which are known or suspected to be caused by viral agents. After dialysis, cancer risk increases 10% to 80% according to studies, with relative risks significantly higher than in the general population, for about 10 cancer sites. There is emerging evidence for an excess risk of cancer in patients in early CKD stages.

Published
2010

32. Molecular determinants of LPS-induced acute renal inflammation: Implication of the kinin B1 receptor

Author

Joost P. Schanstra, Jean-Loup Bascands, Eric Neau, Dimcho Bachvarov, Magdalena Bachvarova, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Cancer Research Centre, Centre Hospitalier Universitaire de Québec-Hôpital L'Hotel-Dieu de Québec, Department of Molecular Medicine, Université Laval [Québec] (ULaval)-Centre Hospitalier Universitaire de Québec, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Simon, Marie Francoise

Subjects
Lipopolysaccharides, MESH: Inflammation, Cytoskeleton organization, Biophysics, Biology, Kidney, Receptor, Bradykinin B1, Biochemistry, MESH: Mice, Knockout, Mice, MESH: Gene Expression Profiling, medicine, Animals, MESH: Animals, Receptor, Cell adhesion, Molecular Biology, MESH: Mice, MESH: Immunity, Oligonucleotide Array Sequence Analysis, Inflammation, Mice, Knockout, MESH: Receptor, Bradykinin B1, MESH: Kidney Diseases, Microarray analysis techniques, Gene Expression Profiling, Immunity, Cell Biology, MESH: Kidney, Kinin, medicine.anatomical_structure, Immunology, Knockout mouse, MESH: Oligonucleotide Array Sequence Analysis, Kidney Diseases, Signal transduction, MESH: Lipopolysaccharides
Abstract

International audience; Acute renal inflammation represents a complex disease and its molecular basis remains incompletely defined. We examined changes of global renal gene expression in lipopolysacharide-treated wild-type and kinin B(1) receptor-knockout mice to better comprehend molecular mechanisms of acute renal inflammation and possible implications of the kinin B(1) receptor in early (inflammatory) stages of renal disease. Microarray data revealed that LPS-mediated renal inflammation is associated with strong induction of gene families that are mostly involved in inflammatory and immune response and cell adhesion, as well as genes associated with metabolism, signal transduction and transport. Downregulated by the LPS challenge were genes and pathways that are necessary for normal renal function, including those implicated in metabolism, transport, protein biosynthesis and, cytoskeleton organization, regulation of transcription and signal transduction. Moreover, we show that B(1) receptor ablation could be protective against inflammation-related kidney injuries.

Published
2009

33. Acute page kidney after a kidney allograft biopsy: successful outcome from observation and medical treatment

Author

Federico Sallusto, Lionel Rostaing, Nassim Kamar, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Néphrologie - Hypertension Artérielle Dialyse - Transplantation, CHU Toulouse [Toulouse]-Hôpital de Rangueil, CHU Toulouse [Toulouse], Service d'Urologie - Transplantation Rénale - Andrologie, Centre de Physiopathologie Toulouse Purpan (CPTP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Département d'Urologie-Andrologie et Transplantation Rénale [CHU Toulouse], Pôle Urologie - Néphrologie - Dialyse - Transplantations - Brûlés - Chirurgie plastique - Explorations fonctionnelles et physiologiques [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), and Simon, Marie Francoise

Subjects
MESH: Signal Transduction, 030232 urology & nephrology, MESH: Genes, p53, 030230 surgery, MESH: Protein Isoforms, MESH: Base Sequence, Bioinformatics, MESH: Hypertension, law.invention, MESH: Kidney Transplantation, MESH: Biopsy, 0302 clinical medicine, law, MESH: Animals, MESH: Tumor Suppressor Protein p53, Zebrafish, MESH: Treatment Outcome, [SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Kidney, Gene knockdown, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, MESH: Radiation Tolerance, MESH: Middle Aged, biology, Page kidney, MESH: Diuresis, MESH: DNA, MESH: Sequence Deletion, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Cell biology, medicine.anatomical_structure, MESH: Acute Disease, Gene isoform, MESH: Zebrafish Proteins, MESH: Creatinine, MESH: Digestive System, MESH: bcl-X Protein, MESH: Animals, Genetically Modified, 03 medical and health sciences, MESH: Promoter Regions, Genetic, medicine, MESH: Diuretics, MESH: Zebrafish, Gene, MESH: RNA, Messenger, MESH: DNA Damage, Transplantation, MESH: Kidney Diseases, MESH: Humans, MESH: Apoptosis, MESH: Feedback, Biochemical, MESH: Genes, Reporter, MESH: Models, Biological, biology.organism_classification, MESH: Male, MESH: Hematoma, Apoptosis, Suppressor, MESH: Transcriptional Activation, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

International audience; p53 is a well-known tumor suppressor and is also involved in processes of organismal aging and developmental control. A recent exciting development in the p53 field is the discovery of various p53 isoforms. One p53 isoform is human Delta133p53 and its zebrafish counterpart Delta113p53. These N-terminal-truncated p53 isoforms are initiated from an alternative p53 promoter, but their expression regulation and physiological significance at the organismal level are not well understood. We show here that zebrafish Delta113p53 is directly transactivated by full-length p53 in response to developmental and DNA-damaging signals. More importantly, we show that Delta113p53 functions to antagonize p53-induced apoptosis via activating bcl2L (closest to human Bcl-x(L)), and knockdown of Delta113p53 enhances p53-mediated apoptosis under stress conditions. Thus, we demonstrate that the p53 genetic locus contains a new p53 response gene and that Delta113p53 does not act in a dominant-negative manner toward p53 but differentially modulates p53 target gene expression to antagonize p53 apoptotic activity at the physiological level in zebrafish. Our results establish a novel feedback pathway that modulates the p53 response and suggest that modulation of the p53 pathway by p53 isoforms might have an impact on p53 tumor suppressor activity.

Published
2009

34. Timing of onset of CKD-related metabolic complications

Author

Moranne, Olivier, Froissart, Marc, Rossert, Jérôme, Gauci, Cédric, Boffa, Jean-Jacques, Haymann, Jean-Philippe, M'Rad, Mona Ben, Jacquot, Christian, Houillier, Pascal, Stengel, Bénédicte, Fouqueray, Bruno, Recherche en épidémiologie et biostatistique, Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de physiologie, explorations fonctionnelles et radioisotopes [CHU HEGP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Paris Descartes - Paris 5 (UPD5)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Faculté de Médecine (UPD5 Médecine), Université Paris Descartes - Paris 5 (UPD5), Remodelage et Reparation du Tissu Renal, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service de Néphrologie et Hémodialyse [CHU HEGP], faculté de médecine, Université Pierre et Marie Curie - Paris 6 (UPMC), The NephroTest Study Group, Université Paris-Sud - Paris 11 ( UP11 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Européen Georges Pompidou [APHP] ( HEGP ), Centre de Recherche des Cordeliers ( CRC (UMR_S 872) ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Université Paris Descartes - Faculté de Médecine ( UPD5 Médecine ), Université Paris Descartes - Paris 5 ( UPD5 ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Service de néphrologie, Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Tenon [APHP], Service de Physiologie [Tenon], Université Pierre et Marie Curie - Paris 6 ( UPMC ), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)

Subjects
metabolic acidosis, MESH: Anemia, MESH: Hyperparathyroidism, MESH : Prevalence, MESH : Male, MESH : Anemia, MESH : Aged, MESH: Acidosis, urologic and male genital diseases, MESH: Hyperphosphatemia, hyperparathyroidism, MESH : Chronic Disease, MESH : Middle Aged, MESH : Female, hyperphosphatemia, MESH: Prevalence, MESH: Aged, MESH: Kidney Diseases, MESH: Middle Aged, MESH: Humans, MESH : Hyperparathyroidism, MESH: Chronic Disease, MESH : Humans, MESH: Time Factors, MESH : Glomerular Filtration Rate, [ SDV.SPEE ] Life Sciences [q-bio]/Santé publique et épidémiologie, MESH: Adult, MESH : Hyperkalemia, MESH : Adult, hyperkalemia, anemia, female genital diseases and pregnancy complications, MESH: Male, MESH: Odds Ratio, MESH: Glomerular Filtration Rate, MESH : Hyperphosphatemia, MESH : Kidney Diseases, MESH: Hyperkalemia, MESH : Odds Ratio, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, MESH : Acidosis, MESH: Female, chronic kidney disease, MESH : Time Factors
Abstract

International audience; Chronic kidney disease (CKD) guidelines recommend evaluating patients with GFR

Published
2009

35. Delayed treatment with plasminogen activator inhibitor-1 decoys reduces tubulointerstitial fibrosis

Author

Sharmila D. Chauhan, Rana Chaaya, Eric Neau, Caroline Nevoit, Jean-Loup Bascands, Julien Gonzalez, Joost P. Schanstra, Julie Klein, Denis Calise, Mathieu Miravete, Christine Delage, Bénédicte Buffin-Meyer, Simon, Marie Francoise, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), IFR 31 Louis Bugnard (IFR 31), and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, MESH: Hepatocyte Growth Factor, Plasmin, MESH: Fibrinolysin, chemistry.chemical_compound, Mice, Fibrosis, MESH: Tissue Plasminogen Activator, Serpin E2, MESH: Fibronectins, MESH: Animals, Fibrinolysin, MESH: Collagen Type III, biology, Hepatocyte Growth Factor, MESH: Peptides, Kidney Tubules, Plasminogen activator inhibitor-1, Tissue Plasminogen Activator, MESH: Fibrosis, MESH: Kidney Tubules, Hepatocyte growth factor, Kidney Diseases, medicine.drug, Ureteral Obstruction, Collagen Type IV, General Biochemistry, Genetics and Molecular Biology, MESH: Urokinase-Type Plasminogen Activator, MESH: Serpins, medicine, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Animals, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Mice, MESH: Collagen Type IV, Serpins, Urokinase, MESH: Kidney Diseases, Macrophages, MESH: Macrophages, medicine.disease, Urokinase-Type Plasminogen Activator, MESH: Male, Fibronectins, Fibronectin, Collagen Type III, chemistry, Immunology, Tubulointerstitial fibrosis, biology.protein, Cancer research, MESH: Ureteral Obstruction, Peptides, Plasminogen activator
Abstract

International audience; We examined the capacity of delayed inhibition of plasminogen activator inhibitor-1 (PAI-1) to reduce tubulointerstitial fibrosis induced by unilateral ureteral obstruction (UUO) in mice. Small peptides mimicking parts of urokinase (uPA) and tissular plasminogen activator (tPA) and serving as decoy molecules for PAI-1 were administered daily during the late stages (3 to 8 days) of UUO. Treatment with PAI-1 decoys reduced interstitial deposition of fibronectin, collagen III and collagen IV without changes in macrophage and myofibroblast infiltration. Interestingly, while PAI-1 activity was reduced and the combined uPA and tPA activity was increased, the antifibrotic effect was obtained without modification of plasmin activity but with increased of hepatocyte growth factor (HGF) expression. We show for the first time that treatment with small PAI-1 decoy peptides reduces established tubulointerstitial fibrosis. This protective effect probably resulted from increased degradation of the extracellular matrix by an HGF dependent mechanism.

Published
2009

36. Delayed blockade of the kinin B1 receptor reduces renal inflammation and fibrosis in obstructive nephropathy

Author

João Bosco Pesquero, Joost P. Schanstra, Eric Neau, Denis Calise, Amrita Ahluwalia, Pierre Carayon, Johan Duchene, Michael Bader, Julie Klein, Laure Esposito, Jean-Philippe Pradère, Christine Delage, Jean-Loup Bascands, Julien Gonzalez, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Fédérale Toulouse Midi-Pyrénées, William Harvey Research Institute, Barts and the London Medical School, Service de Néphrologie - Hypertension Artérielle Dialyse - Transplantation, CHU Toulouse [Toulouse]-Hôpital de Rangueil, CHU Toulouse [Toulouse], IFR 31 Louis Bugnard (IFR 31), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Toulouse [Toulouse]-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Sanofi-Aventis R&D, Sanofi-Aventis, Department of Biophysics, Escola Paulista de Medicina (UNIFESP), UNIFESP, Max Delbrück Center for Molecular Medicine [Berlin] (MDC), and Helmholtz-Gemeinschaft = Helmholtz Association

Subjects
Male, MESH: Inflammation, Pathology, MESH: Sulfonamides, urologic and male genital diseases, Biochemistry, MESH: Mice, Knockout, Mice, Fibrosis, Medicine, MESH: Animals, MESH: Dioxoles, Chemokine CCL7, Renal stem cell, Chemokine CCL2, Mice, Knockout, Sulfonamides, Kinin, MESH: Gene Expression Regulation, MESH: Fibrosis, Kidney Diseases, Biotechnology, MESH: Connective Tissue Growth Factor, medicine.medical_specialty, MESH: Chemokine CCL7, Dioxoles, MESH: Drug Administration Schedule, Drug Administration Schedule, Proinflammatory cytokine, Genetics, Renal fibrosis, Animals, Humans, RNA, Messenger, Molecular Biology, MESH: Chemokine CCL2, MESH: Mice, MESH: RNA, Messenger, Inflammation, MESH: Receptor, Bradykinin B1, MESH: Kidney Diseases, MESH: Humans, business.industry, Connective Tissue Growth Factor, medicine.disease, Obstructive Nephropathy, MESH: Male, Bradykinin B1 Receptor Antagonists, Gene Expression Regulation, business, Tubulointerstitial Disease, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Kidney disease
Abstract

International audience; Renal fibrosis is the common histological feature of advanced glomerular and tubulointerstitial disease leading to end-stage renal disease (ESRD). However, specific antifibrotic therapies to slow down the evolution to ESRD are still absent. Because persistent inflammation is a key event in the development of fibrosis, we hypothesized that the proinflammatory kinin B1 receptor (B1R) could be such a new target. Here we show that, in the unilateral ureteral obstruction model of renal fibrosis, the B1R is overexpressed and that delayed treatment with an orally active nonpeptide B1R antagonist blocks macrophage infiltration, leading to a reversal of the level of renal fibrosis. In vivo bone marrow transplantation studies as well as in vitro studies on renal cells show that part of this antifibrotic mechanism of B1R blockade involves a direct effect on resident renal cells by inhibiting chemokine CCL2 and CCL7 expression. These findings suggest that blocking the B1R is a promising antifibrotic therapy.

Published
2009

37. Chronic kidney disease in children: the National Paediatric Hospital experience in Hanoi, Vietnam

Author

François Bouissou, Nguyen Thi Quynh Huong, Tran Dinh Long, Jean-Loup Bascands, Do Kim Nga, Tran Thi Chien, Dinh Minh Truong, Nguyen Thanh Liem, Simon, Marie Francoise, Department of Paediatric Nephrology, Paediatric National Hospital, Hanoï Medical University, Service de Pédiatrie - Néphrologie, Médecine interne, Hypertension, Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Department of Paediatric Surgery, Biostatistic HIV Training and Research Centre, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Toulouse [Toulouse]-Hôpital des Enfants, CHU Toulouse [Toulouse], and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Nephrology, Male, Pediatrics, medicine.medical_treatment, 030232 urology & nephrology, MESH: Hospitalization, MESH: Kidney Transplantation, 0302 clinical medicine, MESH: Child, MESH: Renal Dialysis, 030212 general & internal medicine, Child, Kidney transplantation, education.field_of_study, General Medicine, MESH: Infant, 3. Good health, Hospitalization, Vietnam, Female, Kidney Diseases, Glomerular Filtration Rate, medicine.medical_specialty, Adolescent, Population, Peritoneal dialysis, End stage renal disease, MESH: Social Class, 03 medical and health sciences, Renal Dialysis, Internal medicine, medicine, Humans, Renal replacement therapy, education, MESH: Adolescent, MESH: Kidney Diseases, MESH: Humans, business.industry, MESH: Chronic Disease, Infant, medicine.disease, Kidney Transplantation, MESH: Male, Transplantation, MESH: Glomerular Filtration Rate, Social Class, Chronic Disease, MESH: Vietnam, business, MESH: Female, Kidney disease
Abstract

International audience; AIM: The goal of this descriptive study was to evaluate the aetiology and the socioeconomic status in hospitalized children in Hanoi and propose solutions to improve prevention and basic health care of patients with chronic kidney disease in Hanoi City. METHODS: The records of all 152 hospitalized children with chronic kidney disease in the National Paediatric Hospital in Hanoi from January 2001 to December 2005 were analyzed. RESULTS: The incidence of paediatric chronic kidney disease native to Hanoi City was estimated to be 5.1/million-child population (pmcp). Median age was 11.29 years; 60.5% were boys and 39.5% were girls; 65% of patients were in end-stage renal disease. Causes of chronic kidney disease included glomerulonephritis (66.4%) and congenital/hereditary anomalies (13%). In 19.8% of children, the aetiology was unavailable. During hospitalization, five patients died and 76 patients (50%) refused the treatment although beneficiaries of health insurance. Thirty patients (19.74%) received peritoneal dialysis and haemodialysis, and seven patients received renal transplantation with a familial living donor. CONCLUSION: Late referral, and limited facilities for renal replacement therapy explain the poor outcome in this study. We need a program to delineate the burden of chronic kidney disease and improve primary health care for health promotion and prevention of paediatric chronic kidney disease.

Published
2009

38. [Anti-CD10 fetomaternal alloimmunisation]

Author

Pierre, Ronco, Hanna, Debiec, Vincent, Guigonis, CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Physiologie Moléculaire de la Réponse Immune et des Lymphoproliférations (PMRIL), and Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Centre National de la Recherche Scientifique (CNRS)

Subjects
MESH: Carcinoma, MESH: Combined Modality Therapy, Placenta, MESH: Maternal-Fetal Exchange, MESH: Pregnancy, Pregnancy, MESH: Podocytes, Humans, Maternal-Fetal Exchange, MESH: Kidney Diseases, MESH: Humans, Podocytes, MESH: Neprilysin, fungi, MESH: Adenocarcinoma, MESH: Adult, MESH: Placenta, Adoptive Transfer, MESH: Vulvar Neoplasms, Fetal Diseases, MESH: Adoptive Transfer, MESH: Fetal Diseases, MESH: Vaginal Neoplasms, MESH: Immunization, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Immunization, Kidney Diseases, Neprilysin, MESH: Female
Abstract

International audience; Fetomaternal alloimmunization with antenatal glomerulopathies (FMAIG) is a recently described alloimmune disorder, which results from the production of maternal antibodies that cross the placenta, bind to fetal glomerular podocytes, and mediate renal disease. The pathogenic antibodies are directed against CD10/neutral endopeptidase (NEP). The infant's mother is NEP-deficient and thus she becomes immunized during the first pregnancy against CD10/NEP expressed by placental cells. Because future pregnancies in CD10/NEP-immunized mothers are at high risk for the fetus, detection of anti-NEP antibodies in pregnant mothers and antigen-driven therapies including induction of tolerance, are urgently needed. This ideally requires identification of the pathogenic epitopes born by the antigen and specifically recognized by B- and T-cells. We have recently characterized such epitopes that will be used in diagnostic tests (ELISA) and for new therapeutic approaches based on peptide-specific immune intervention. For this purpose, we have developed an experimental model by crossing NEP/CD10-deficient female mice to wild-type males. The females develop an alloimmune reaction against NEP, which is a prerequisite for tolerance induction experiments. Although NEP/CD10 does not seem to be involved in common idiopathic forms of membranous nephropathy in the adult, alloimmune antibodies may be implicated in de novo membranous nephropathy that develop in the kidney graft and after alloimmune bone marrow transplantation.

Published
2009

39. Timing of onset of CKD-related metabolic complications.: Onset of CKD-Related Metabolic Complications

Author

Moranne, Olivier, Froissart, Marc, Rossert, Jérôme, Gauci, Cédric, Boffa, Jean-Jacques, Haymann, Jean-Philippe, M'Rad, Mona Ben, Jacquot, Christian, Houillier, Pascal, Stengel, Bénédicte, Fouqueray, Bruno, De Lauzon-Guillain, Blandine, Recherche en épidémiologie et biostatistique, Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de physiologie, explorations fonctionnelles et radioisotopes [CHU HEGP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Faculté de Médecine (UPD5 Médecine), Université Paris Descartes - Paris 5 (UPD5), Remodelage et Reparation du Tissu Renal, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service de Néphrologie et Hémodialyse [CHU HEGP], faculté de médecine, Université Pierre et Marie Curie - Paris 6 (UPMC), and The NephroTest Study Group

Subjects
metabolic acidosis, MESH: Anemia, MESH: Hyperparathyroidism, MESH: Acidosis, urologic and male genital diseases, MESH: Hyperphosphatemia, hyperparathyroidism, hyperphosphatemia, MESH: Prevalence, MESH: Aged, MESH: Kidney Diseases, MESH: Middle Aged, MESH: Humans, MESH: Chronic Disease, MESH: Time Factors, MESH: Adult, hyperkalemia, anemia, female genital diseases and pregnancy complications, MESH: Male, MESH: Odds Ratio, MESH: Glomerular Filtration Rate, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, MESH: Hyperkalemia, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, MESH: Female, chronic kidney disease
Abstract

International audience; Chronic kidney disease (CKD) guidelines recommend evaluating patients with GFR

Published
2009

40. [Functional MR urography in children]

Author

P H, Vivier, E, Blondiaux, M, Dolores, N, Marouteau-Pasquier, M, Brasseur, C, Petitjean, J N, Dacher, Laboratoire d'Informatique, de Traitement de l'Information et des Systèmes (LITIS), Université Le Havre Normandie (ULH), Normandie Université (NU)-Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Institut national des sciences appliquées Rouen Normandie (INSA Rouen Normandie), Institut National des Sciences Appliquées (INSA)-Normandie Université (NU)-Institut National des Sciences Appliquées (INSA), Service d'imagerie médicale [CHU Rouen], Hôpital Charles Nicolle [Rouen]-CHU Rouen, Normandie Université (NU), Breton, Céline, Hôpital Charles Nicolle [Rouen], CHU Rouen, and Normandie Université (NU)-Normandie Université (NU)-CHU Rouen

Subjects
Adult, Gadolinium DTPA, Male, Urologic Diseases, MESH: Gadolinium DTPA, Contrast Media, MESH: Magnetic Resonance Angiography, Hydronephrosis, urologic and male genital diseases, MESH: Magnetic Resonance Imaging, Young Adult, MESH: Urography, MESH: Furosemide, Sex Factors, MESH: Sex Factors, Furosemide, MESH: Contrast Media, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Diuretics, Diuretics, MESH: Age Factors, MESH: Kidney Diseases, MESH: Humans, Body Weight, MESH: Child, Preschool, Age Factors, Infant, Urography, MESH: Adult, Magnetic Resonance Imaging, MESH: Hydronephrosis, MESH: Infant, MESH: Male, MESH: Urologic Diseases, MESH: Body Weight, MESH: Young Adult, Child, Preschool, Female, Kidney Diseases, MESH: Female, Magnetic Resonance Angiography
Abstract

International audience; MR Urography (MRU) provides both morphologic and functional information without radiation exposure. It enables the assessment of split renal function, excretion, and quantification of obstruction. MRU is thus complementary to ultrasonography in the assessment of pre- and post-natal obstructive uropathies in children. If available, MRU should be definitely preferred to intravenous urography.

Published
2009

41. Morbidity of retropubic radical prostatectomy for prostate cancer in renal transplant recipients: multicenter study from Renal Transplantation Committee of French Urological Association

Author

Jacques Petit, François Kleinclauss, Nicolas Terrier, G. Guichard, Yann Neuzillet, Eric Lechevallier, Xavier Tillou, Comité de transplantation rénale, Association Française d'Urologie, Service d'urologie, andrologie et transplantation rénale, Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Hôpital Saint-Jacques, Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS BFC)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Service d'urologie et de transplantation rénale, Université de la Méditerranée - Aix-Marseille 2-Assistance Publique - Hôpitaux de Marseille (APHM), Service d'urologie, CHU Amiens-Picardie, Département Urologie, CHU Grenoble, Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), Saas, Philippe, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Franche-Comté (UFC), and Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])

Subjects
Male, Nephrology, medicine.medical_treatment, 030232 urology & nephrology, MESH: Kidney Transplantation, 0302 clinical medicine, MESH: Treatment Outcome, MESH: Urologic Surgical Procedures, MESH: Aged, education.field_of_study, MESH: Middle Aged, Prostatectomy, Middle Aged, 3. Good health, Treatment Outcome, 030220 oncology & carcinogenesis, Urologic Surgical Procedures, [SDV.IMM]Life Sciences [q-bio]/Immunology, Kidney Diseases, France, medicine.medical_specialty, [SDV.IMM] Life Sciences [q-bio]/Immunology, Urology, Urinary system, Population, 03 medical and health sciences, MESH: Prostatectomy, Internal medicine, medicine, Humans, education, Aged, Retrospective Studies, MESH: Kidney Diseases, MESH: Humans, business.industry, Prostatic Neoplasms, Retrospective cohort study, MESH: Retrospective Studies, medicine.disease, Kidney Transplantation, MESH: Urology, MESH: Male, Surgery, Transplantation, MESH: France, MESH: Prostatic Neoplasms, business, Kidney cancer, Kidney disease
Abstract

International audience; OBJECTIVES: To evaluate the morbidity and surgical complications of retropubic radical prostatectomy (RRP) in renal transplant recipients (RTRs) and compare these results with the observed morbidity in a control group of nontransplanted patients. METHODS: We conducted a multicenter retrospective study and reviewed the charts and records of 20 RTRs who had undergone RRP for localized prostate cancer at four French renal transplant centers belonging to the Renal Transplantation Committee of the French Urological Association from April 1996 to April 2007. A total of 40 patients who had undergone RRP at the same centers, by the same surgeons, were analyzed as the case-control population. RESULTS: The mean operating time (163 +/- 41 vs 160 +/- 66 minutes), blood loss (516 +/- 279 vs 566 +/- 449 mL), transfusion rate (20% vs 22.5%), and hospital stay (11.9 +/- 5.44 vs 9.45 +/- 2.8 days) were similar in the RTR and case-control populations. No graft loss or graft injury was reported in the RTRs, except for two ureteral injuries that were immediately repaired during RRP. No decrease in the kidney graft function was observed after RRP. The rate of medical complication (deep venous thrombosis, pulmonary embolism, urinary tract infection) was similar in both groups, except for the rate of bacterial systemic infection, which was significantly greater in the RTRs than in the controls (15% vs 2.5%, P = .01). CONCLUSIONS: In our study, RRP was a safe procedure to treat localized prostate cancer in RTRs. RRP resulted in the same morbidity in RTRs as in the case-control population.

Published
2008

42. CDK/GSK-3 inhibitors as therapeutic agents for parenchymal renal diseases

Author

S.H. Obligado, Anna Zuk, Peter J. Nelson, O. Ibraghimov-Beskrovnaya, L. Meijer, Molécules et cibles thérapeutiques (MCT), Station biologique de Roscoff [Roscoff] (SBR), Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), and Oregon State University (OSU)

Subjects
Nephrology, medicine.medical_specialty, proliferation, Lupus nephritis, End stage renal disease, immunology, Glycogen Synthase Kinase 3, Mice, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Polycystic kidney disease, Animals, Humans, MESH: Protein Kinase Inhibitors, MESH: Animals, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Protein Kinase Inhibitors, MESH: Mice, 030304 developmental biology, MESH: Glycogen Synthase Kinase 3, 0303 health sciences, Kidney, MESH: Kidney Diseases, end-stage renal disease, MESH: Humans, business.industry, Acute kidney injury, apoptosis, MESH: Biological Markers, medicine.disease, Cyclin-Dependent Kinases, 3. Good health, medicine.anatomical_structure, MESH: Cyclin-Dependent Kinases, 030220 oncology & carcinogenesis, Immunology, Cancer research, Mesangial proliferative glomerulonephritis, Kidney Diseases, business, Biomarkers, chronic kidney disease, Kidney disease
Abstract

Drug discovery to lessen the burden of chronic renal failure and end-stage renal disease remains a principle goal of translational research in nephrology. In this review, we provide an overview of the current development of small molecule cyclin-dependent kinase (CDK)/glycogen synthase kinase-3 (GSK-3) inhibitors as therapeutic agents for parenchymal renal diseases. The emergence of this drug family has resulted from the recognition that CDKs and GSK-3s play critical roles in the progression and regression of many kidney diseases. CDK/GSK-3 inhibitors suppress pathogenic proliferation, apoptosis, and inflammation, and promote regeneration of injured tissue. Preclinical efficacy has now been demonstrated in mesangial proliferative glomerulonephritis, crescentic glomerulonephritis, collapsing glomerulopathy, proliferative lupus nephritis, polycystic kidney diseases, diabetic nephropathy, and several forms of acute kidney injury. Novel biomarkers of therapy are aiding the process of drug development. This review will highlight these advancements in renal therapeutics.

Published
2008

43. Ureteral stent placement and BK virus allograft nephropathy in renal transplant recipients

Author

Didier Ducloux, Amir Kazory, Service d'urologie, andrologie et transplantation rénale, Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Hôpital Saint-Jacques, Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté]), Saas, Philippe, Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), and Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)

Subjects
medicine.medical_specialty, [SDV.IMM] Life Sciences [q-bio]/Immunology, MESH: Polyomavirus Infections, 030232 urology & nephrology, Urology, 030230 surgery, medicine.disease_cause, MESH: Kidney Transplantation, 03 medical and health sciences, 0302 clinical medicine, Allograft nephropathy, medicine, ComputingMilieux_MISCELLANEOUS, MESH: Treatment Outcome, Transplantation, MESH: Kidney Diseases, MESH: Humans, business.industry, 3. Good health, BK virus, Stent placement, MESH: Stents, Renal transplant, MESH: Ureter, [SDV.IMM]Life Sciences [q-bio]/Immunology, business
Abstract

International audience

Published
2008

44. Lysophosphatidic acid and renal fibrosis

Author

Jean-Philippe Pradere, David J. Salant, Joost P. Schanstra, Sandra Grès, Philippe Valet, Julie Klein, Jean-Loup Bascands, Jean-Sébastien Saulnier-Blache, Julien Gonzalez, Saulnier-Blache, Jean Sébastien, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Medicine, and Boston University [Boston] (BU)

Subjects
medicine.medical_treatment, Connective tissue, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Biology, Models, Biological, Article, MESH: Lysophospholipids, chemistry.chemical_compound, Fibrosis, Pulmonary fibrosis, Lysophosphatidic acid, medicine, Renal fibrosis, MESH: Receptors, Lysophosphatidic Acid, Animals, Humans, MESH: Animals, Receptors, Lysophosphatidic Acid, Receptor, Molecular Biology, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, Kidney, MESH: Kidney Diseases, MESH: Humans, Growth factor, MESH: Models, Biological, Cell Biology, medicine.disease, medicine.anatomical_structure, chemistry, Immunology, MESH: Fibrosis, Cancer research, Kidney Diseases, Lysophospholipids
Abstract

International audience; The development of fibrosis involves a multitude of events and molecules. Until now the majority of these molecules were found to be proteins or peptides. But recent data show significant involvement of the phospholipid lysophosphatidic acid (LPA) in the development of pulmonary, liver and renal fibrosis. The latest data on the role of LPA and the G-protein-coupled LPA1 receptor in the development of renal fibrosis will be discussed. LPA1-receptor activation was found to be associated with increased vascular leakage and increased fibroblast recruitment in pulmonary fibrosis. Furthermore, in renal fibrosis LPA1-receptor activation stimulates macrophage recruitment and connective tissue growth factor expression. The observations make this receptor an interesting alternative and new therapeutic target in fibrotic diseases.

Published
2008

45. [Effects of smoking on the thyroid gland, digestive system, kidney and bone]

Author

Underner, M., Hadjadj, S., Beauchant, M., Bridoux, Franck, Debiais, F., Meurice, J.-C., Carrion, Claire, Physiologie Moléculaire de la Réponse Immune et des Lymphoproliférations (PMRIL), and Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Centre National de la Recherche Scientifique (CNRS)

Subjects
MESH: Kidney Diseases, MESH: Smoking, MESH: Humans, [SDV.IMM] Life Sciences [q-bio]/Immunology, Digestive System Diseases, Smoking, Thyroid Diseases, MESH: Digestive System Diseases, Risk Factors, MESH: Risk Factors, Humans, MESH: Thyroid Diseases, [SDV.IMM]Life Sciences [q-bio]/Immunology, Kidney Diseases, MESH: Bone Diseases, Bone Diseases
Abstract

International audience; INTRODUCTION: In addition to being a major cardiovascular risk factor, smoking promotes or worsens thyroid, digestive, renal and bone diseases. BACKGROUND: Smoking is positively associated with hyperthyroidism. It is associated with Graves' disease and it especially increases the risk of the development of severe exophthalmos. In contrast, smoking might exert a protective action for thyroid carcinoma. Smoking increases the severity of hepatic lesions in patients with chronic hepatitis C. Smoking accelerates the progression of primary biliary cirrhosis and increases the risk of hepatocellular carcinoma. Smoking increases risk of both hyperplastic and adenomatous polyps. While Crohn's disease is associated with smoking, ulcerative colitis is largely a disease of non smokers. Smoking increases risk of development of both renal cell carcinoma and chronic nephropathies, particularly in types 1 and 2 diabetes. Smoking is a risk factor for decreased bone density and is associated with a significantly increased risk of fracture. Smoking is related to the development of rheumatoid arthritis and may adversely influence its severity. CONCLUSIONS: Smoking might be considered a risk factor for the development of several thyroid, digestive, renal and bone diseases. Consequently, smoking prevention and cessation programs must be strongly encouraged among the patients concerned.

Published
2008

46. [Management of renal colic in pregnant women, based on a series of 48 cases]

Author

Guichard, Guillaume, Fromajoux, C., Cellarier, Damien, Loock, Pierre-Yves, Chabannes, Eric, Bernardini, Stéphane, Maillet, Robert, Bittard, Hugues, Kleinclauss, François, Service de Néphrologie et Urologie, Centre Hospitalier Régional Universitaire [Besançon] ( CHRU Besançon ) -Hôpital Saint-Jacques, Service de gynécologie, Carcinogénèse épithéliale : facteurs prédictifs et pronostiques - UFC ( CEF2P / CARCINO ), Centre Hospitalier Régional Universitaire [Besançon] ( CHRU Besançon ) -Université Bourgogne Franche-Comté ( UBFC ) -Université de Franche-Comté ( UFC ), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC ( HOTE GREFFON ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Etablissement français du sang [Bourgogne-France-Comté] ( EFS [Bourgogne-France-Comté] ) -Université de Franche-Comté ( UFC ), Service d'urologie, andrologie et transplantation rénale, Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Hôpital Saint-Jacques, Carcinogénèse épithéliale : facteurs prédictifs et pronostiques - UFC (EA 3181) (CEF2P / CARCINO), Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté]), Carcinogénèse épithéliale : facteurs prédictifs et pronostiques - UFC (UR 3181) (CEF2P / CARCINO), Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), and Saas, Philippe

Subjects
Adult, Colic, [SDV.IMM] Life Sciences [q-bio]/Immunology, MESH : Retrospective Studies, Pain, MESH : Pregnancy Complications, Fetal Distress, MESH: Adrenal Cortex Hormones, MESH: Urinary Calculi, MESH : Adrenal Cortex Hormones, MESH: Pregnancy, Adrenal Cortex Hormones, Pregnancy, Humans, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, MESH : Female, Retrospective Studies, MESH: Kidney Diseases, MESH: Humans, MESH: Colic, MESH : Humans, MESH : Urinary Calculi, MESH : Colic, MESH: Adult, MESH: Retrospective Studies, MESH: Fetal Distress, MESH : Adult, Pregnancy Complications, MESH : Pregnancy, MESH : Fetal Distress, MESH: Pregnancy Complications, MESH : Kidney Diseases, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Kidney Diseases, Urinary Calculi, MESH: Pain, MESH: Female, MESH : Pain
Abstract

International audience; INTRODUCTION: Urinary stones are relatively frequent in pregnant women and raise specific diagnostic and therapeutic problems. The authors conducted a retrospective review of the management of this disease in their establishment. PATIENTS AND METHODS: Between January 1999 and December 2003, out of a total of 10,398 parturients, 48 pregnant women were hospitalised for renal colic, that is, incidence of 0.04%. The medical records of these patients were retrospectively reviewed and clinical, laboratory, treatment and outcome data were analysed. RESULTS: Standard analgesic treatment, comprising paracetamol and an antispasmodic, achieved pain relief in 84% of cases. A concomitant short course of corticosteroid therapy in cases of renal colic refractory to standard treatment was effective in 71% of patients and allowed deferral of surgical management in five out of seven cases. A double J stent was placed in all patients requiring urinary diversion, followed by closer ultrasound and bacteriological monitoring throughout pregnancy. Only two patients required surgical management of their stone after delivery. The only obstetric event related to renal colic was induction of labour at term in two cases because of foetal distress. CONCLUSION: The authors propose a two-stage management plan for renal colic in pregnant women resulting in a low maternal and foetal complication rate.

Published
2008

47. Clinical and histological characteristics of renal AA amyloidosis: a retrospective study of 68 cases with a special interest to amyloid-associated inflammatory response. : Clinical and histological characteristics of renal AA amyloidosis

Author

Verine, Jérôme, Mourad, Nathalie, Desseaux, Kristell, Vanhille, Philippe, Noël, Laure-Hélène, Beaufils, Hélène, Grateau, Gilles, Janin, Anne, Droz, Dominique, Service d'anatomo-pathologie [Paris], Assistance publique - Hôpitaux de Paris (AP-HP)-Université Paris Diderot - Paris 7 ( UPD7 ) -Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Gvh et Gvl : Physiopathologie Chez l'Homme et Chez l'Animal, Incidence et Role Therapeutique, Université Paris Diderot - Paris 7 ( UPD7 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Service d'informatique médicale, Service de médecine interne et néphrologie, CH Valenciennes, Mecanismes de l'Inflammation et de l'Adherence Cellulaire Dans les Maladies Renales, Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Service d'anatomie pathologique neurologique, Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Pitié-Salpêtrière [APHP], Service de médecine interne, Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Tenon [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'anatomie pathologique neurologique [CHU Pitié-Salpêtrière], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), CHU Tenon [AP-HP], and Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
MESH: Inflammation, [ SDV.MHEP.UN ] Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, MESH: Serum Amyloid A Protein, MESH : Retrospective Studies, MESH : Hematuria, Inflammatory reaction, MESH : Male, Histological forms, MESH : Aged, urologic and male genital diseases, Kidney, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, MESH: Hypertension, MESH: Proteinuria, AA amyloidosis, MESH: Amyloidosis, MESH : Middle Aged, MESH : Female, MESH: Hematuria, MESH: Aged, MESH: Kidney Diseases, MESH: Middle Aged, MESH: Humans, MESH : Proteinuria, MESH : Serum Amyloid A Protein, MESH : Inflammation, urogenital system, MESH : Humans, MESH : Hypertension, MESH: Adult, MESH: Retrospective Studies, MESH : Adult, MESH: Male, Glomerular crescents, MESH : Amyloidosis, MESH : Kidney Diseases, MESH: Female
Abstract

International audience; We retrospectively reviewed the clinicopathological features of a series of 68 renal AA amyloidosis observations collected between 1990 and 2005. The amyloidogenic disease was a chronic infection (40.8%), a chronic inflammation (38%), a tumor (9.9%), a hereditary disease (9.9%), or was undetermined in 1.4% of cases. Nephrotic syndrome and renal insufficiency were noted in 63.1% and 75% of patients, respectively. The distribution pattern of glomerular amyloid deposits was mesangial segmental (14.7%), mesangial nodular (26.5%), mesangiocapillary (32.3%), and hilar (26.5%). Glomerular form was observed in 80.9% of cases and vascular form in 19.1%. AA amyloidosis-related inflammation was noted in 30 patients (44.1%) and appeared as a multinucleated giant cell reaction (27.9%) or a glomerular inflammatory infiltrate (25%), including glomerular crescents (17.6%). At the end of follow-up, 26 patients (38.2%) showed end-stage renal disease. The clinical presentation of glomerular and vascular forms was distinct with a clear predominance of proteinuria in glomerular form. Inflammatory reaction was preferentially observed in biopsies with a codeposition of immunoglobulin chains and/or complement factors in AA amyloid deposits. The distribution pattern of glomerular amyloid deposits and glomerular inflammatory reaction were independent factors influencing proteinuria level. Tubular atrophy, abundance, and distribution pattern of glomerular amyloid deposits at the time of biopsy were independent predictors of renal outcome. In conclusion, the glomerular involvement appeared as the determining histological factor for clinical manifestations and outcome of renal AA amyloidosis. AA amyloidosis-related inflammation could partly result from an immune response directed against AA fibrils and could induce amyloid resolution and crescents.

Published
2007

48. Long-term outcomes after coronary artery bypass grafting: preoperative kidney function is prognostic

Author

Michel Chonchol, Tomas Berl, Marc Laskar, Philippe Lacroix, Victor Aboyans, Gerard Smits, Neuroépidémiologie Tropicale et Comparée (NETEC), Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Institut d'Epidémiologie Neurologique et de Neurologie Tropicale-Université de Limoges (UNILIM), Service de Chirurgie Thoracique et Vasculaire - Médecine vasculaire [CHU Limoges], and CHU Limoges

Subjects
Male, Time Factors, medicine.medical_treatment, 030204 cardiovascular system & hematology, Kidney, 0302 clinical medicine, Risk Factors, MESH: Risk Factors, 030212 general & internal medicine, Coronary Artery Bypass, Stroke, MESH: Treatment Outcome, MESH: Aged, Hazard ratio, Prognosis, 3. Good health, Treatment Outcome, Cardiology, Female, Kidney Diseases, Cardiology and Cardiovascular Medicine, Pulmonary and Respiratory Medicine, MESH: Preoperative Care, Acute coronary syndrome, medicine.medical_specialty, Renal function, Revascularization, Preoperative care, MESH: Prognosis, 03 medical and health sciences, Internal medicine, Preoperative Care, medicine, Humans, Aged, MESH: Kidney Diseases, MESH: Humans, business.industry, MESH: Chronic Disease, MESH: Coronary Artery Bypass, MESH: Time Factors, Perioperative, MESH: Kidney, medicine.disease, MESH: Male, Chronic Disease, Surgery, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, business, MESH: Female, Kidney disease
Abstract

International audience; OBJECTIVE: End-stage renal disease is an independent predictor of mortality after coronary artery bypass grafting. Limited information exists, however, regarding the impact of chronic kidney disease on long-term outcome after bypass grafting. The purpose of this study was to assess the impact of kidney function on long-term outcomes in patients undergoing coronary artery bypass grafting. METHODS: We studied 931 consecutive patients undergoing coronary artery bypass grafting in a single center. Demographic and clinical data were collected preoperatively. Chronic kidney disease was defined preoperatively according to the Modification of Diet in Renal Disease equation as an estimated glomerular filtration rate less than 60 mL x min(-1) x 1.73 m(-2). Multivariate Cox proportional hazard analyses were performed to determine the independent prognostic factors after bypass grafting. The primary outcome was a composite, combining death, acute coronary syndrome, stroke or transient ischemic attack, and coronary or peripheral revascularization during follow-up. Secondary outcomes were overall causes of death and cardiovascular death, acute coronary syndrome, and stroke or transient ischemic attack. RESULTS: One hundred fourteen (12.2%) patients had preoperative chronic kidney disease (estimated glomerular filtration rate range, 20.5-59.8 mL x min(-1) x 1.73 m(-2)). After a mean follow-up of 3.1 +/- 1.4 years (median, 3.3 years), chronic kidney disease was found to be an independent predictor of the composite outcome (hazard ratio and 95% confidence interval, 1.46 [1.01-2.11]; P = .0467) and overall death (hazard ratio and 95% confidence interval, 1.89 [1.16-3.07]; P = .0106). CONCLUSIONS: Beyond the perioperative period, preoperative moderate-to-severe chronic kidney disease is an independent long-term predictor of cardiovascular events and total mortality after coronary artery bypass grafting. Chronic kidney disease status should be incorporated into prediction models and clinical risk assessments.

Published
2007

49. [Renal and urinary tract disease national research program]

Author

Stengel, Bénédicte, Antignac, Corinne, Baverel, Gabriel, Choukroun, Gabriel, Cussenot, Olivier, Dussaule, Jean-Claude, Friedlander, Gérard, Lang, Philippe, Lelièvre-Pégorier, Martine, Massy, Ziad, Monteiro, Renato, Parini, Angelo, Soulillou, Jean Paul, Baud, Laurent, Ronco, Pierre, Recherche en épidémiologie et biostatistique, Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM), Neuropathies héréditaires et rein en développement, Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Métabolomique et maladies métaboliques, Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM), Faculté de médecine, RTH Laennec, Université de Picardie Jules Verne (UPJV), CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre de Recherche Saint-Antoine (UMRS893), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de recherche Croissance et signalisation (UMR_S 845), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Hôpital Henri Mondor, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Paris Descartes - Paris 5 (UPD5)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Affectations Mineralisantes du Systeme Cardiovasculaire : Calcifications Arterielles et Valvulaires Aortiques, Université de Picardie Jules Verne (UPJV)-Institut National de la Santé et de la Recherche Médicale (INSERM), Immunopathologie rénale, récepteurs et inflammation, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de transplantation et de recherche en transplantation (ITERT), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN), Immunointervention dans les allo et xénotransplantations, Université de Nantes (UN)-IFR26-Institut National de la Santé et de la Recherche Médicale (INSERM)-ITUN, Remodelage et Reparation du Tissu Renal, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Toulouse (UT)-Université de Toulouse (UT)- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Simon, Marie Francoise, Université Paris-Sud - Paris 11 ( UP11 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université de Picardie, CHU Amiens-Picardie, CHU Tenon [APHP], Centre de Recherche Saint-Antoine ( CR Saint-Antoine ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Centre de recherche Croissance et signalisation ( UMR_S 845 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), Centre de Recherche des Cordeliers ( CRC (UMR_S 872) ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Université de Picardie Jules Verne ( UPJV ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université Paris Diderot - Paris 7 ( UPD7 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut de médecine moléculaire de Rangueil ( I2MR ), Université Toulouse III - Paul Sabatier ( UPS ), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut de transplantation et de recherche en transplantation ( ITERT ), Université de Nantes ( UN ), and Université de Nantes ( UN ) -IFR26-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -ITUN

Subjects
Urologic Diseases, MESH: Kidney Diseases, MESH: Humans, MESH : Urologic Diseases, Incidence, Research, MESH : Foundations, MESH : Humans, MESH : Research, Kidney Transplantation, MESH : Incidence, MESH: Urologic Diseases, MESH: Kidney Transplantation, MESH: France, MESH: Research, MESH: Foundations, MESH : Kidney Diseases, Humans, MESH : Kidney Transplantation, Kidney Diseases, France, MESH: Incidence, MESH : France, Foundations
Abstract

International audience; The National Institute of Health and Medical Research (Inserm), the Society of Nephrology, and the French Kidney Foundation recognized the need to create a National Research Program for kidney and urinary tract diseases. They organized a conference gathering 80 researchers to discuss the state-of-the art and evaluate the strengths and weaknesses of kidney and urinary tract disease research in France, and to identify research priorities. From these priorities emerged 11 of common interest: 1) conducting epidemiologic studies; 2) conducting large multicenter cohorts of well-phenotyped patients with blood, urine and biopsy biobanks; 3) developing large scale approach: transcriptomics, proteomics, metabolomics; 4) developing human and animal functional imaging techniques; 5) strengthening the expertise in renal pathology and electrophysiology; 6) developing animal models of kidney injury; 7) identifying nontraumatic diagnostic and prognostic biomarkers; 8) increasing research on the fetal programming of adult kidney diseases; 9) encouraging translational research from bench to bedside and to population; 10) creating centers grouping basic and clinical research workforces with critical mass and adequate logistic support; 11) integrating and developing european research programs.

Published
2007

50. Clinical and histological characteristics of renal AA amyloidosis: a retrospective study of 68 cases with a special interest to amyloid-associated inflammatory response.: Clinical and histological characteristics of renal AA amyloidosis

Author

Verine, Jérôme, Mourad, Nathalie, Desseaux, Kristell, Vanhille, Philippe, Noël, Laure-Hélène, Beaufils, Hélène, Grateau, Gilles, Janin, Anne, Droz, Dominique, Ratajczak, Philippe, Service d'anatomo-pathologie [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Gvh et Gvl : Physiopathologie Chez l'Homme et Chez l'Animal, Incidence et Role Therapeutique, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'informatique médicale, Service de médecine interne et néphrologie, CH Valenciennes, Mecanismes de l'Inflammation et de l'Adherence Cellulaire Dans les Maladies Renales, Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'anatomie pathologique neurologique [CHU Pitié-Salpêtrière], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), CHU Tenon [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)

Subjects
MESH: Aged, MESH: Inflammation, MESH: Kidney Diseases, MESH: Middle Aged, MESH: Humans, MESH: Serum Amyloid A Protein, urogenital system, Inflammatory reaction, Histological forms, MESH: Adult, MESH: Retrospective Studies, urologic and male genital diseases, Kidney, [SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, Glomerular crescents, MESH: Hypertension, MESH: Male, MESH: Proteinuria, AA amyloidosis, MESH: Amyloidosis, MESH: Female, MESH: Hematuria
Abstract

International audience; We retrospectively reviewed the clinicopathological features of a series of 68 renal AA amyloidosis observations collected between 1990 and 2005. The amyloidogenic disease was a chronic infection (40.8%), a chronic inflammation (38%), a tumor (9.9%), a hereditary disease (9.9%), or was undetermined in 1.4% of cases. Nephrotic syndrome and renal insufficiency were noted in 63.1% and 75% of patients, respectively. The distribution pattern of glomerular amyloid deposits was mesangial segmental (14.7%), mesangial nodular (26.5%), mesangiocapillary (32.3%), and hilar (26.5%). Glomerular form was observed in 80.9% of cases and vascular form in 19.1%. AA amyloidosis-related inflammation was noted in 30 patients (44.1%) and appeared as a multinucleated giant cell reaction (27.9%) or a glomerular inflammatory infiltrate (25%), including glomerular crescents (17.6%). At the end of follow-up, 26 patients (38.2%) showed end-stage renal disease. The clinical presentation of glomerular and vascular forms was distinct with a clear predominance of proteinuria in glomerular form. Inflammatory reaction was preferentially observed in biopsies with a codeposition of immunoglobulin chains and/or complement factors in AA amyloid deposits. The distribution pattern of glomerular amyloid deposits and glomerular inflammatory reaction were independent factors influencing proteinuria level. Tubular atrophy, abundance, and distribution pattern of glomerular amyloid deposits at the time of biopsy were independent predictors of renal outcome. In conclusion, the glomerular involvement appeared as the determining histological factor for clinical manifestations and outcome of renal AA amyloidosis. AA amyloidosis-related inflammation could partly result from an immune response directed against AA fibrils and could induce amyloid resolution and crescents.

Published
2007

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