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2. Étude PROspective, Multicentrique, randomisée, en ouvert, évaluant le bénéfice sur la fonction rénale à 12 mois post-transplantation, d’une immunosuppression avec sevrage de l’inhibiteur de la calcineurine à 3 mois et associant mycophénolate sodique-Evérolimus versus Tacrolimus-Evérolimus chez des patients transplantés rénaux de novo

Author

Thierry, A., primary, Anglicheau, D., additional, Buchler, M., additional, Lemoine, M., additional, Ohlmann, S., additional, Colosio, C., additional, Ecotière, L., additional, Touchard, G., additional, Goujon, J.M., additional, and Ragot, S., additional

Published
2022
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8. Les Auteurs

Author

Abroug, F., Abtan, J., Aguilar, C., Aissaoui, N., Ait Hssain, A., Ait-Oufella, H., Ajzenberg, N., Aloy, B., Ammirati, C., Amoura, Z., Amstutz, P., Anglicheau, D., Annane, D., Anxionnat, R., Arab, K., Argaud, L., Arnaout, M., Arrivé, L., Assouad, J., Aubron, C., Augis, V., Ayari, H., Azabou, E., Azoulay, E., Bakhos, D., Bailly, E., Bailly, P., Baldolli, A., Barbaud, A., Barbier, F., Barbut, F., Bardon, J., Barraud, D., Barreda, T., Barrot, L., Barry, B., Bartier, J.-C., Bastien, O., Baud, F.J., Baudel, J.-L., Beaussier, M., Bedos, J.-P., Bédry, R., Béduneau, G., Beloncle, F., Beltrami, A., Benghanem, S., Ben Ammar, M., Ben Hadj Salem, O., Benchetrit, D., Benyamina, M., Benzidi, Y., Bernardin, G., Bertholdt, C., Bertocchio, J.-P., Bertoletti, L., Bertrand, C., Besnier, E., Beuret, P., Beydon, L., Bialais, É., Bienaimé, F., Bigé, N., Bihan, K., Bilbault, P., Binoche, A., Biour, M., Birgand, G., Bitker, L., Blanc, J.-V., Blatteau, J.-E., Blivet, S., Blot, F., Bodenes, L., Boels, D., Bohé, J., Boissier, F., Boiteau, R., Boles, J.-M., Bollaert, P.-E., Bondeelle, L., Bonnet, N., Boudon, M., Bouglé, A., Boulain, T., Boulanger, D., Bounab, R., Bourcier, S., Bourigault, C., Bourenne, J., Bouteau, I., Boutonnet, M., Bouzgarrou, R., Boyer, A., Boyer, D., Boyer-Suavet, S., Bracard, S., Brault, C., Bretonnière, C., Bréchot, N., Bridoux, F., Brivet, F.-G., Brochard, L., Bruder, N., Bruneel, F., Brunet, J., Burgel, P.-R., Buscot, M., Cabrio, D., Cadranel, J., Calvet, L., Camus, C., Canaud, B., Canellas, A., Canet, E., Capaldo, L., Capellier, G., Carbonell, N., Cariou, A., Carli, P., Carpentier, D., Carrat, F., Carteaux, G., Casolla, B., Castanares-Zapatero, D., Castelain, V., Cavaillon, J.-M., Cecchini, J., Cha, O., Chamaraux-Tran, T.-N., Champigneulle, B., Chanard, J., Charles, P.-E., Charpentier, J., Chastre, J., Chaussard, M., Chemla, D., Cherifa, M., Chiche, J.-D., Cholley, B., Chopin, C., Chosidow, O., Choukroun, M.-L., Clair, B., Claude, F., Clavier, T., Clément, E., Clere-Jehl, R., Clouzeau, B., Cochereau, I., Cohen, Y., Collins, M., Combes, A., Commandeur, D., Contou, D., Coppo, P., Cordonnier, C., Coriat, P., Cornelis, F., Costedoat-Chalumeau, N., Cottin, V., Cour, M., Coutrot, M., Couturier, J., Couzigou, C., Cravoisy-Popovic, A., Crozier, S., Danel, V., Danin, P.-E., Dargaud, Y., Darmaun, D., Darmon, M., Daubin, C., David, S., De Backer, D., De Cagny, B., Decavèle, M., Decousus, H., Degos, V., De Groote, E., De Jong, A., Dekeyser, T., Delabranche, X., Delahaye, A., Delarue, J., Delclaux, C., Delemazure, J., Delile, E., Delisle, S., Dellamonica, J., Delluc, A., Delplancq, H., Deltour, S., De Martin, E., Demeret, S., Demiselle, J., De Montalembert, M., Demoule, A., Dépret, F., de Prost, N., Dequatre-Ponchelle, N., Dequin, P.-F., Deray, G., Derelle, A.-L., Deriaz, H., De Schryver, N., Deshayes, S., Desmettre, T., Desrousseaux, J., Dessevre, A., Dewitte, A., Deye, N., Dhainaut, J.-F., Didier, S., Diehl, J.-L., Di Martino, V., Djibré, M., Dolz, M., Dorandeu, F., Dorent, R., Do Vale, J., Dres, M., Dreyfuss, D., Dromer, C., Dubée, V., Duburcq, T., Duceau, B., Du Cheyron, D., Ducloy-Bouthors, A.-S., Dugernier, J., Durand, A., Durand, F., Duranteau, J., Durocher, A., Dussaule, J.-C., Eckert, C., Écotière, L., Ehrmann, S., El Gharbi, F., Elbaz, M., Embriaco, N., Étienne, H., Essig, M., Fagon, J.-Y., Fagot-Gandet, F., Fartoukh, M., Faugeras, F., Favory, R., Faisy, C., Ferrière, N., Ferry, T., Flamant, M., Folscheid, D., Fontaine, E., Forel, J.-M., Fourrier, F, Fraipont, V., Franchineau, G., Francoz, C., Frat, J.-P., Fresco, R., Friedlander, G., Friedman, D., Fromentin, M., Gainnier, M., Galanaud, D., Garcia, H., Garret, C., Garrouste-Orgeas, M., Gateau, C., Geeraerts, T., Gehanno, P., Gempp, E., Geri, G., Germain, A., Giacardi, C., Gibelin, A., Gibot, S., Girardot, T., Girault, C., Giura, G., Gkalea, V., Godard, A., Godeau, B., Goffinet, F., Gonzalez-Bermejo, J., Gory, B., Gouëllo, J.-P., Goulenok, C., Goursaud, S., Goury, A., Goutagny, S., Graftieaux, J.-P., Grangé, S., Grimaldi, D., Gros, A., Gruson, D., Gruson-Vescovali, D., Guérin, C., Guérot, E., Guettrot-Imbert, G., Guervilly, C., Guidet, B., Guillon, A., Guillot, M., Guitton, C., Gutton, Ch., Haidar, M., Halimi, C., Hamada, S., Hammoud, K., Hansmann, Y., Hariri, G., Harlay, M.-L., Harrois, A., Harry, P., Hauw-Berlemont, C., Hébuterne, X., Hejblum, G., Helms, J., Hékimian, G., Heming, N., Herbrecht, J.-E., Hertig, A., Heshmati, F., Hickmann, C., Hites, M., Hong Tuan Ha, V., Houfflin-Debarge, V., Houhou, N., Houillier, P., Hua, C., Hullin, T., Humbert, M., Hugon-Vallet, É., Hurel, D., Ichaï, P., Ioos, V., Isnard-Bagnis, C., Jaber, S., Jacobs, F., Jacquens, A., Jaffal, K., Jaïs, X., Janus, N., Jardel, B., Jars-Guincestre, M.-C., Jaubert, P., Jehl, F., Jirka, A., Joannès-Boyau, O., Joffre, J., Jolliet, P., Joly, F., Joly, L.-M., Joly-Guillou, M.-L., Jouffroy, R., Jonard, M., Jougon, J., Jourdain, M., Jozwiak, M., Jully, M., Jung, B., Juniat, A.-A., Kandji, M., Kanfer, A., Karoubi, P., Kentish-Barnes, N., Kerlan, V., Khalil, A., Kim, S., Kimmoun, A., Klouche, K., Koffel, J.-C., Kopferschmitt, J., Laaban, J.P., Labadie, M., Labbé, V., Lachâtre, M., Labrousse, J., Lacroix, D., Lancel, S., Lanceleur, A., Landais, M., Landelle, C., Landman, C., Lanternier, F., Larcher, R., Launay-Vacher, V., Langeron, O., Lapostolle, F., Larmignat, P., Laterre, P.-F., Laudenbach, V., Laurent, V., Lautrette, A., Lavillegrand, J.-R., Lavolé, A., Law-ye, B., Lebas, B., Lebranchu, Y., Lebreton, G., Lebrun-Vignes, B., Leclercq, D., Le Conte, P., Le Corre, B., Lefaucheur, J.-P., Lefevre, J., Leflon-Guibout, V., Léger, D., Legrand, M., Le Gouez, A., Leguay, T., Lejay, M., Lellouche, F., Lemaire, F., Lemaitre, C., Lemarié, J., Lemiale, V., Lemonnier, M.-P., Lepape, A., Leprince, P., Leray-Moraguès, H., Léon, A., Leone, M., Lerolle, N., Le Roux, M., Leroy, O., Leteurtre, S., Lescot, T., Le Tulzo, Y., Leverve, X., Levy, B., Lévy, P., L'Her, E., Liao, L., Lienhart, A., Llitjos, J.-F., Lofaso, F., Lothe, M.-N., Loubières, Y., Louge, P., Lucet, J.-C., Luyt, C.E., Lyazidi, A., Maamar, A., Mahieu, R., Maillet, J.-M., Mainardi, J.-L., Maître, B., Maizel, J., Mallaret, M.-R., Mancebo, J., Manzo-Silberman, S., Marchalot, A., Marit, G., Markowicz, P., Marqué, S., Martin, O., Martin-Lefèvre, L., Marx, T., Massanet, P.L., Mathian, A., Mathieu, C., Mathieu, D., Maury, E., Maxime, V., Mazeraud, A., Meffert, A., Mégarbane, B., Mehl, J., Mekontso Dessap, A., Melchior, C., Meng, P., Mentec, H., Mercier, F.-J., Mercat, A., Merdji, H., Méresse, Z., Mertes, P.-M., Mesland, J.-B., Meyer, G., Meynard, J.-L., Meziani, F., Miatello, J., Michard, B., Mira, J.-P., Mismetti, P., Misset, B., Miyara, M., Moga, L., Mohty, M., Monchi, M., Monéger, G., Monneret, G., Monnet, X., Monnier-Cholley, L., Montani, D., Mora, P., Morau, E., Moreau, AS., Morel, G., Morawiec, E., Mortaza, S., Mottier, D., Murgier, M., Naccache, L., Nace, L., Naeije, R., Naïm, G., Nave, S., Nitenberg, A., Nouette-Gaulain, K., Nouri-Neuville, M., Nousbaum, J.B., Novy, E., Nuss, P., Obadia, É., Offenstadt, G., Oger, E., Onimus, T., Orlikowski, D., Oro, S., Osman, O., Ouanes, I., Ouanes-Besbes, L., Ouedraogo, R., Outin, H., Oziel, J., Ozier, Y., Pajot, O., Papazian, L., Parmentier, E., Parquin, F., Parrilla, F.J., Parrot, A., Pasquet, A., Pateron, D., Paugam-Burtz, C., Peigné, M., Peineau, S., Pelaccia, T., Pène, F., Perrotin, D., Pessey, F., Pham, T., Philit, F., Pichené, C., Picod, A., Piette, J.-C., Pillet, O., Pilmis, B., Pineau, J., Pineton de Chambrun, M., Piquilloud, L., Pirracchio, R., Piton, G., Plantefève, G., Podglajen, I., Poidevin, A., Poissy, J., Pottecher, J., Poujol, A.-L., Poussardin, C., Prat, F., Préau, S., Preiser, J.-C., Prevel, R., Prot-Bertoye, C., Pruvo, J.-P., Pujol, S., Puntous, M., Quenot, J.-P., Quevrain, E., Quillerou, B., Rabaud, C., Raynard, B., Raynaud, L., Regard, L., Reignier, J., Reizine, F., Réminiac, F., Renault, A., Revest, M., Ricard, J.-D., Richalet, J-P., Richard, C., Richard, J-C.M., Ricôme, J.-L., Ridel, C., Rigollot, M., Rigaud, J.-P., Rigolet, A., Rimmelé, T., Rineau, E., Robert, R., Robert, T., Robineau, O., Roch, A., Roesler, J., Roger, I., Rohaut, B., Roullet, S., Rousset, D., Roux, D., Rozé, H., Rudler, M., Rugeri, L., Ruppé, E., Sab, J.-M., Sacleux, S.-C., Saliba, F., Samuel, D., Sauder, P., Saulnier, F., Sauvanet, A., Savale, L., Savoye, G., Schlemmer, B., Schlemmer, F., Schmidt, E., Schmidt, M., Schneider, F., Schneider, S.M., Schortgen, F., Schuby, M., Schwan, R., Schwebel, C., Seguin, A., Seksik, P., Senneville, É., Seronde, M.-F., Sharshar, T., Sigaut, S., Silva, S., Si-Tahar, M., Sitbon, O., Sivanandamoorthy, S., Slama, M., Sollet, J.-P., Somme, D., Sonneville, R., Souday, V., Soufir, L., Soussi, S., Souweine, B., Spaulding, C., Squara, P., Steg, P.-G., Sterlin, D., Stiel, L., Sublon, M., Sudre, E., Surgers, L., Szychowiak, P., Tacquard, C., Tadié, J.-M., Talvard, O., Tamburini, J., Tamion, F., Tarazona, V., Tardy, B., Taright, N., Tasseau, F., Tattevin, P., Tauzin-Fin, P., Tazarourte, K., Teboul, J.-L., Terzi, N., Thabut, D., Thaler, F., Thellier, D., Thervet, E., Thévenot, T., Thibault, M., Thibault, R., Thierry, A., Thille, A.W., Thomas, G., Thumerel, M., Thuong, M., Thy, M., Timsit, J.-F., Tissières, P., Tonnelet, R., Touchard, G., Tournoy, A., Tourtier, J.-P., Tourtier, Y., Tran Van Nhieu, J., Troché, G., Trouillet, J.L., Ubeaud-Séquier, G., Uhel, F., Urbina, T., Valeyrie-Allanore, L., Van de Louw, A., Van der Meersch, G., Vargas, F., Velly, L., Venet, F., Verdon, R., Veyradier, A., Vieillard-Baron, A., Vignon, Ph., Vigué, B., Villers, D., Vinsonneau, C., Voiriot, G., Weil-Verhoeven, D., Wiel, É., Wittebole, X., Woch, S., Woerther, P.-L., Woimant, F., Wolff, M., Wysocki, M., Xhaard, A., Yazdanpanah, Y., Zafrani, L., Zahar, J.-R., Zarrouk, V., Zéni, F., Zerbib, P., Zerbib, Y., Zieleskiewicz, L., Zlotnik, D., and Zuber, B.

Published
2020
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16. Impact of Calcineurin Inhibitor-Based Immunosuppression Maintenance During the Dialysis Period After Kidney Transplant Failure on the Next Kidney Graft Outcome: A Retrospective Multicenter Study With Propensity Score Analysis.

Author

Noelle J, Mayet V, Lambert C, Couzi L, Chauveau B, Thierry A, Ecotière L, Bertrand D, Laurent C, Lemal R, Grèze C, Freist M, Heng AE, Rouzaire PO, and Garrouste C

Subjects
Humans, Calcineurin Inhibitors therapeutic use, Immunosuppressive Agents therapeutic use, Immunosuppressive Agents pharmacology, Propensity Score, Graft Rejection prevention & control, Renal Dialysis, Kidney, Immunosuppression Therapy, Graft Survival, Kidney Transplantation, Kidney Diseases
Abstract

The impact of immunosuppressive therapy (IS) strategies after kidney transplant failure (KTF) on potential future new grafts is poorly established. We assessed the potential benefit of calcineurin inhibitor (CNI)-based IS maintenance throughout the dialysis period on the outcome of the second kidney transplant (KT). We identified 407 patients who underwent a second KT between January 2008 and December 2018 at four French KT centers. Inverse probability of treatment weighting was used to control for potential confounding. We included 205 patients with similar baseline characteristics at KTF: a total of 53 received at least CNIs on the retransplant day (G-CNI), and 152 did not receive any IS (G-STOP). On the retransplant date, G-STOP patients experienced a longer pretransplant dialysis time, were more often hyperimmunized, and underwent more expanded-criteria donor KTs than G-CNI patients. During the second KT follow-up period, rejection episodes were similar in both groups. The 10-year survival rates without death and dialysis were 98.7% and 59.5% in G-CNI and G-STOP patients, respectively. In the multivariable analysis, CNI-based IS maintenance was associated with better survival (hazard ratio: 0.08; 95% confidence interval: 0.01-0.58, p = 0.01). CNI-based IS maintenance throughout the dialysis period after KTF may improve retransplantation outcomes., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Noelle, Mayet, Lambert, Couzi, Chauveau, Thierry, Ecotière, Bertrand, Laurent, Lemal, Grèze, Freist, Heng, Rouzaire and Garrouste.)

Published
2023
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17. Diagnosis and risk factors for intracranial aneurysms in autosomal polycystic kidney disease: a cross-sectional study from the Genkyst cohort.

Author

Lefèvre S, Audrézet MP, Halimi JM, Longuet H, Bridoux F, Ecotière L, Augusto JF, Duveau A, Renaudineau E, Vigneau C, Frouget T, Charasse C, Gueguen L, Perrichot R, Couvrat G, Seret G, Le Meur Y, and Cornec-Le Gall E

Subjects
Humans, Female, Male, Aged, Cross-Sectional Studies, Risk Factors, Estrogens, Intracranial Aneurysm complications, Intracranial Aneurysm epidemiology, Polycystic Kidney, Autosomal Dominant complications, Polycystic Kidney, Autosomal Dominant diagnosis, Polycystic Kidney, Autosomal Dominant epidemiology, Polycystic Kidney Diseases complications, Polycystic Kidney Diseases diagnosis, Polycystic Kidney Diseases epidemiology
Abstract

Background: Autosomal dominant polycystic kidney disease (ADPKD) is associated with an increased risk for developing intracranial aneurysms (IAs). We aimed to evaluate the frequency of diagnosis of IAs in the cross-sectional, population-based, Genkyst cohort, to describe ADPKD-associated IAs and to analyse the risk factors associated with the occurrence of IAs in ADPKD patients., Methods: A cross-sectional study was performed in 26 nephrology centres from the western part of France. All patients underwent genetic testing for PKD1/PKD2 and other cystogenes., Results: Among the 2449 Genkyst participants, 114 (4.65%) had a previous diagnosis of ruptured or unruptured IAs at inclusion, and ∼47% of them had a positive familial history for IAs. Most aneurysms were small and saccular and located in the anterior circulation; 26.3% of the patients had multiple IAs. The cumulative probabilities of a previous diagnosis of IAs were 3.9%, 6.2% and 8.1% at 50, 60 and 70 years, respectively. While this risk appeared to be similar in male and female individuals <50 years, after that age, the risk continued to increase more markedly in female patients, reaching 10.8% versus 5.4% at 70 years. The diagnosis rate of IAs was >2-fold higher in PKD1 compared with PKD2, with no influence of PKD1 mutation type or location. In multivariate analysis, female sex, hypertension <35 years, smoking and PKD1 genotype were associated with an increased risk for diagnosis of IAs., Conclusions: This study presents epidemiological data reflecting real-life clinical practice. The increased risk for IAs in postmenopausal women suggests a possible protective role of oestrogen., (© The Author(s) 2022. Published by Oxford University Press on behalf of the ERA.)

Published
2022
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18. PKD2-Related Autosomal Dominant Polycystic Kidney Disease: Prevalence, Clinical Presentation, Mutation Spectrum, and Prognosis.

Author

Cornec-Le Gall E, Audrézet MP, Renaudineau E, Hourmant M, Charasse C, Michez E, Frouget T, Vigneau C, Dantal J, Siohan P, Longuet H, Gatault P, Ecotière L, Bridoux F, Mandart L, Hanrotel-Saliou C, Stanescu C, Depraetre P, Gie S, Massad M, Kersalé A, Séret G, Augusto JF, Saliou P, Maestri S, Chen JM, Harris PC, Férec C, and Le Meur Y

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Cross-Sectional Studies, Disease Progression, Female, Humans, Male, Middle Aged, Polycystic Kidney, Autosomal Dominant complications, Prognosis, Renal Insufficiency, Chronic etiology, Young Adult, Mutation, Polycystic Kidney, Autosomal Dominant diagnosis, Polycystic Kidney, Autosomal Dominant genetics, TRPP Cation Channels genetics
Abstract

Background: PKD2-related autosomal dominant polycystic kidney disease (ADPKD) is widely acknowledged to be of milder severity than PKD1-related disease, but population-based studies depicting the exact burden of the disease are lacking. We aimed to revisit PKD2 prevalence, clinical presentation, mutation spectrum, and prognosis through the Genkyst cohort., Study Design: Case series, January 2010 to March 2016., Settings & Participants: Genkyst study participants are individuals older than 18 years from 22 nephrology centers from western France with a diagnosis of ADPKD based on Pei criteria or at least 10 bilateral kidney cysts in the absence of a familial history. Publicly available whole-exome sequencing data from the ExAC database were used to provide an estimate of the genetic prevalence of the disease., Outcomes: Molecular analysis of PKD1 and PKD2 genes. Renal survival, age- and sex-adjusted estimated glomerular filtration rate., Results: The Genkyst cohort included 293 patients with PKD2 mutations (203 pedigrees). PKD2 patients with a nephrology follow-up corresponded to 0.63 (95% CI, 0.54-0.72)/10,000 in Brittany, while PKD2 genetic prevalence was calculated at 1.64 (95% CI, 1.10-3.51)/10,000 inhabitants in the European population. Median age at diagnosis was 42 years. Flank pain was reported in 38.9%; macroscopic hematuria, in 31.1%; and cyst infections, in 15.3% of patients. At age 60 years, the cumulative probability of end-stage renal disease (ESRD) was 9.8% (95% CI, 5.2%-14.4%), whereas the probability of hypertension was 75.2% (95% CI, 68.5%-81.9%). Although there was no sex influence on renal survival, men had lower kidney function than women. Nontruncating mutations (n=36) were associated with higher age-adjusted estimated glomerular filtration rates. Among the 18 patients with more severe outcomes (ESRD before age 60), 44% had associated conditions or nephropathies likely to account for the early progression to ESRD., Limitations: Younger patients and patients presenting with milder forms of PKD2-related disease may not be diagnosed or referred to nephrology centers., Conclusions: Patients with PKD2-related ADPKD typically present with mild disease. In case of accelerated degradation of kidney function, a concomitant nephropathy should be ruled out., (Copyright © 2017 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Published
2017
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20. Minimization of maintenance immunosuppressive therapy after renal transplantation comparing cyclosporine A/azathioprine or cyclosporine A/mycophenolate mofetil bitherapy to cyclosporine A monotherapy: a 10-year postrandomization follow-up study.

Author

Thierry A, Le Meur Y, Ecotière L, Abou-Ayache R, Etienne I, Laurent C, Vuiblet V, Colosio C, Bouvier N, Aldigier JC, Rerolle JP, Javaugue V, Gand E, Bridoux F, Essig M, Hurault de Ligny B, and Touchard G

Subjects
Adult, Azathioprine adverse effects, Cyclosporins adverse effects, Drug Therapy, Combination, Female, Follow-Up Studies, Graft Rejection, Graft Survival, Humans, Immunosuppression Therapy methods, Immunosuppressive Agents adverse effects, Kidney Transplantation adverse effects, Kidney Transplantation methods, Male, Middle Aged, Mycophenolic Acid administration & dosage, Mycophenolic Acid adverse effects, Prospective Studies, Risk Assessment, Statistics, Nonparametric, Survival Analysis, Time Factors, Treatment Outcome, Azathioprine administration & dosage, Cyclosporins administration & dosage, Immunosuppressive Agents administration & dosage, Kidney Transplantation mortality, Maintenance Chemotherapy methods, Mycophenolic Acid analogs & derivatives
Abstract

Long-term outcomes in renal transplant recipients withdrawn from steroid and submitted to further minimization of immunosuppressive regimen after 1 year are lacking. In this multicenter study, 204 low immunological risk kidney transplant recipients were randomized 14.2 ± 3.7 months post-transplantation to receive either cyclosporine A (CsA) + azathioprine (AZA; n = 53), CsA + mycophenolate mofetil (MMF; n = 53), or CsA monotherapy (n = 98). At 3 years postrandomization, the occurrence of biopsy for graft dysfunction was similar in bitherapy and monotherapy groups (21/106 vs. 26/98; P = 0.25). At 10 years postrandomization, patients' survival was 100%, 94.2%, and 95.8% (P = 0.25), and death-censored graft survival was 94.9%, 94.7%, and 95.2% (P = 0.34) in AZA, MMF, and CsA groups, respectively. Mean estimated glomerular filtration rate was 70.4 ± 31.1, 60.1 ± 22.2, and 60.1 ± 19.0 ml/min/1.73 m(2), respectively (P = 0.16). The incidence of biopsy-proven acute rejection was 1.4%/year in the whole cohort. None of the patients developed polyomavirus-associated nephropathy. The main cause of graft loss (n = 12) was chronic antibody-mediated rejection (n = 6). De novo donor-specific antibodies were detected in 13% of AZA-, 21% of MMF-, and 14% of CsA-treated patients (P = 0.29). CsA monotherapy after 1 year is safe and associated with prolonged graft survival in well-selected renal transplant recipient (ClinicalTrials.gov number: 980654)., (© 2015 Steunstichting ESOT.)

Published
2016
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21. Kidney diseases associated with monoclonal immunoglobulin M-secreting B-cell lymphoproliferative disorders: a case series of 35 patients.

Author

Chauvet S, Bridoux F, Ecotière L, Javaugue V, Sirac C, Arnulf B, Thierry A, Quellard N, Milin S, Bender S, Goujon JM, Jaccard A, Fermand JP, and Touchard G

Subjects
Acute Kidney Injury etiology, Acute Kidney Injury immunology, Acute Kidney Injury pathology, Adult, Aged, Aged, 80 and over, Amyloid immunology, Amyloidosis etiology, Amyloidosis immunology, Amyloidosis pathology, Antibodies, Monoclonal immunology, Cohort Studies, Female, Glomerulonephritis, Membranoproliferative etiology, Glomerulonephritis, Membranoproliferative immunology, Glomerulonephritis, Membranoproliferative pathology, Humans, Kidney Diseases immunology, Kidney Diseases pathology, Kidney Neoplasms immunology, Kidney Neoplasms pathology, Lymphoma, B-Cell immunology, Lymphoma, B-Cell pathology, Lymphoproliferative Disorders complications, Lymphoproliferative Disorders immunology, Male, Middle Aged, Nephritis, Interstitial etiology, Nephritis, Interstitial immunology, Nephritis, Interstitial pathology, Nephrotic Syndrome etiology, Nephrotic Syndrome immunology, Nephrotic Syndrome pathology, Paraproteinemias immunology, Paraproteinemias pathology, Retrospective Studies, Waldenstrom Macroglobulinemia immunology, Waldenstrom Macroglobulinemia pathology, B-Lymphocytes immunology, Immunoglobulin M immunology, Kidney Diseases etiology, Kidney Neoplasms complications, Lymphoma, B-Cell complications, Paraproteinemias complications, Waldenstrom Macroglobulinemia complications
Abstract

Background: Kidney diseases associated with immunoglobulin M (IgM) monoclonal gammopathy are poorly described, with few data for patient outcomes and renal response., Study Design: Case series., Setting & Participants: 35 patients from 8 French departments of nephrology were retrospectively studied. Inclusion criteria were: (1) detectable serum monoclonal IgM, (2) estimated glomerular filtration rate (eGFR) < 60mL/min/1.73m(2) and/or proteinuria with protein excretion > 0.5g/d and/or microscopic hematuria, and (3) kidney biopsy showing monoclonal immunoglobulin deposits and/or lymphomatous B-cell renal infiltration. All patients received chemotherapy, including rituximab-based regimens in 8 cases., Predictors: Patients were classified into 3 groups according to renal pathology: glomerular AL amyloidosis (group 1; n=11), nonamyloid glomerulopathies (group 2; n=15, including 9 patients with membranoproliferative glomerulonephritis), and tubulointerstitial nephropathies (group 3; n=9, including cast nephropathy in 5, light-chain Fanconi syndrome in 3, and isolated tumor infiltration in 1)., Outcomes: Posttreatment hematologic response (≥50% reduction in serum monoclonal IgM and/or free light chain level) and renal response (≥50% reduction in 24-hour proteinuria or eGFR≥30mL/min/1.73m(2) in patients with glomerular and tubulointerstitial disorders, respectively)., Results: Nephrotic syndrome was observed in 11 and 6 patients in groups 1 and 2, respectively. Patients in group 3 presented with acute kidney injury (n=7) and/or proximal tubular dysfunction (n=3). Waldenström macroglobulinemia was present in 26 patients (8, 12, and 6 in groups 1, 2, and 3, respectively). Significant lymphomatous interstitial infiltration was observed in 18 patients (4, 9, and 5 patients, respectively). Only 9 of 29 evaluable patients had systemic signs of symptomatic hematologic disease (2, 5, and 2, respectively). In groups 1, 2, and 3, respectively, hematologic response was achieved after first-line treatment in 3 of 9, 9 of 10, and 5 of 6 evaluable patients, while renal response occurred in 5 of 10, 9 of 15, and 5 of 8 evaluable patients., Limitations: Retrospective study; insufficient population to establish the impact of chemotherapy., Conclusions: IgM monoclonal gammopathy is associated with a wide spectrum of renal manifestations, with an under-recognized frequency of tubulointerstitial disorders., (Copyright © 2015 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Published
2015
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