10 results on '"Huelin P"'
Search Results
2. Ellagic acid and its metabolites urolithins A/B ameliorate most common disease phenotypes in cellular and mouse models for lysosomal storage disorders by enhancing extracellular vesicle secretion
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Beatriz Soto-Huelin, Bohdan Babiy, Oscar Pastor, Mario Díaz-García, Ana Toledano-Zaragoza, María Dolores Frutos, Juan Carlos Espín, Francisco A. Tomás-Barberán, Rebeca Busto, and María Dolores Ledesma
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Extracellular vesicles ,Polyphenols ,Lysosomal storage disorders ,Niemann pick ,Brain ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Niemann Pick diseases types A (NPDA) and C (NPDC) are lysosomal storage disorders (LSDs) leading to cognitive impairment, neurodegeneration, and early death. NPDA and NPDC have different genetic origins, being caused by mutations in the acid sphingomyelinase (ASM) or the cholesterol transport protein NPC1, respectively. However, they share a common pathological hallmark in the accumulation of lipids in the endolysosomal compartment. Here, we tested the hypothesis that polyphenols reduce lipid overload in NPD cells by enhancing the secretion of extracellular vesicles (ECVs). We show that among the polyphenols tested, the ellagic acid metabolites, urolithin A and B, were the safest and most efficient in increasing ECV secretion. They reduced levels of accumulating lipids and lysosomal size and permeabilization in cultured bone marrow-derived macrophages and neurons from ASMko and NPC1 mutant mice, which mimic NPDA and NPDC, respectively. Moreover, oral treatment with ellagic acid reduced lipid levels, ameliorated lysosomal alterations, and diminished microglia activation in the brain of NPD mice. These results support the therapeutic value of ECV secretion and polyphenols for NPDs, which may also help treat other LSDs characterized by intracellular lipid overload.
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- 2023
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3. Molecular characterization of chronic liver disease dynamics: From liver fibrosis to acute-on-chronic liver failure
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Isabel Graupera, Laura Isus, Mar Coll, Elisa Pose, Alba Díaz, Julia Vallverdú, Teresa Rubio-Tomás, Celia Martínez-Sánchez, Patricia Huelin, Marta Llopis, Cristina Solé, Elsa Solà, Constantino Fondevila, Juan José Lozano, Pau Sancho-Bru, Pere Ginès, and Patrick Aloy
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chronic liver disease ,ACLF ,network biology ,temporal gene expression profile ,biomarker ,Diseases of the digestive system. Gastroenterology ,RC799-869 - Abstract
Background & Aims: The molecular mechanisms driving the progression from early-chronic liver disease (CLD) to cirrhosis and, finally, acute-on-chronic liver failure (ACLF) are largely unknown. Our aim was to develop a protein network-based approach to investigate molecular pathways driving progression from early-CLD to ACLF. Methods: Transcriptome analysis was performed on liver biopsies from patients at different liver disease stages, including fibrosis, compensated cirrhosis, decompensated cirrhosis and ACLF, and control healthy livers. We created 9 liver-specific disease-related protein-protein interaction networks capturing key pathophysiological processes potentially related to CLD. We used these networks as a framework and performed gene set-enrichment analysis (GSEA) to identify dynamic gene profiles of disease progression. Results: Principal component analyses revealed that samples clustered according to the disease stage. GSEA of the defined processes showed an upregulation of inflammation, fibrosis and apoptosis networks throughout disease progression. Interestingly, we did not find significant gene expression differences between compensated and decompensated cirrhosis, while ACLF showed acute expression changes in all the defined liver disease-related networks. The analyses of disease progression patterns identified ascending and descending expression profiles associated with ACLF onset. Functional analyses showed that ascending profiles were associated with inflammation, fibrosis, apoptosis, senescence and carcinogenesis networks, while descending profiles were mainly related to oxidative stress and genetic factors. We confirmed by qPCR the upregulation of genes of the ascending profile and validated our findings in an independent patient cohort. Conclusion: ACLF is characterized by a specific hepatic gene expression pattern related to inflammation, fibrosis, apoptosis, senescence and carcinogenesis. Moreover, the observed profile is significantly different from that of compensated and decompensated cirrhosis, supporting the hypothesis that ACLF should be considered a distinct entity. Lay summary: By using transjugular biopsies obtained from patients at different stages of chronic liver disease, we unveil the molecular pathogenic mechanisms implicated in the progression of chronic liver disease to cirrhosis and acute-on-chronic liver failure. The most relevant finding in this study is that patients with acute-on-chronic liver failure present a specific hepatic gene expression pattern distinct from that of patients at earlier disease stages. This gene expression pattern is mostly related to inflammation, fibrosis, angiogenesis, and senescence and apoptosis pathways in the liver.
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- 2022
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4. Neutrophil gelatinase-associated lipocalin is a biomarker of acute-on-chronic liver failure and prognosis in cirrhosis
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Ariza Cardenal, Javier, Graupera, Isabel, Coll, M., Solà, Elsa, Barreto, R., García, E., Moreira, Rebeca, Elia, Chiara, Morales Ruiz, Manuel, Llopis, M., Huelin, Patricia, Solé Padullés, Cristina, Fabrellas i Padrès, Núria, Weiss, E., Nevens, Frederick, Gerbes, A. L. (Alexander L.), Trebicka, Jonel, Saliba, Faouzi, Fondevila Campo, Constantino, Hernández Gea, Virginia, Fernández, J., Bernardi, Mauro, Arroyo, Vicente, Jiménez Povedano, Wladimiro, Deulofeu, Carme, Pavesi, Marco, Angeli, Paolo, Jalan, Rajiv, Moreau, Richard, Sancho Bru, Pau, Ginès i Gibert, Pere, CANONIC Investigators, EASL CLIF Consortium, Universitat de Barcelona, Ariza, X, Graupera, I, Coll, M, Solà, E, Barreto, R, García, E, Moreira, R, Elia, C, Morales-Ruiz, M, Llopis, M, Huelin, P, Solé, C, Fabrellas, N, Weiss, E, Nevens, F, Gerbes, A, Trebicka, J, Saliba, F, Fondevila, C, Hernández-Gea, V, Fernández, J, Bernardi, M, Arroyo, V, Jiménez, W, Deulofeu, C, Pavesi, M, Angeli, P, Jalan, R, Moreau, R, Sancho-Bru, P, and Ginès, P
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0301 basic medicine ,Liver Cirrhosis ,medicine.medical_specialty ,Cirrhosis ,Cirrosi hepàtica ,Pronòstic mèdic ,Renal function ,Lipocalin ,Systemic inflammation ,Gastroenterology ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Lipocalin-2 ,Acute-on-chronic liver failure ,Biomarker ,NGAL ,Hepatology ,Internal medicine ,medicine ,Humans ,Liver injury ,Creatinine ,Neutrophil gelatinase-associated lipocalin ,business.industry ,Acute kidney injury ,Liver failure ,Acute-On-Chronic Liver Failure ,Acute Kidney Injury ,medicine.disease ,Prognosis ,030104 developmental biology ,chemistry ,Hepatic cirrhosis ,Immunology ,Biomarker (medicine) ,030211 gastroenterology & hepatology ,Insuficiència hepàtica ,medicine.symptom ,business ,Biomarkers ,cirrhosi - Abstract
BACKGROUND & AIMS: Acute-on-chronic liver failure (ACLF) is a syndrome that occurs in cirrhosis characterized by organ failure(s) and high mortality rate. There are no biomarkers of ACLF. The LCN2 gene and its product, neutrophil gelatinase-associated lipocalin (NGAL), are upregulated in experimental models of liver injury and cultured hepatocytes as a result of injury by toxins or proinflammatory cytokines, particularly Interleukin-6. The aim of this study was to investigate whether NGAL could be a biomarker of ACLF and whether LCN2 gene may be upregulated in the liver in ACLF. METHODS: We analyzed urine and plasma NGAL levels in 716 patients hospitalized for complications of cirrhosis, 148 with ACLF. LCN2 expression was assessed in liver biopsies from 29 additional patients with decompensated cirrhosis with and without ACLF. RESULTS: Urine NGAL was markedly increased in ACLF vs. no ACLF patients (108(35-400) vs. 29(12-73)μg/g creatinine; p
- Published
- 2016
5. Development of chronic kidney disease after acute kidney injury in patients with cirrhosis is common and impairs clinical outcomes.
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Bassegoda O, Huelin P, Ariza X, Solé C, Juanola A, Gratacós-Ginès J, Carol M, Graupera I, Pose E, Napoleone L, Albertos S, de Prada G, Cervera M, Fernández J, Fabrellas N, Poch E, Solà E, and Ginès P
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- Acute Kidney Injury blood, Acute Kidney Injury epidemiology, Aged, Creatinine blood, Female, Follow-Up Studies, Glomerular Filtration Rate, Humans, Liver Cirrhosis blood, Liver Cirrhosis epidemiology, Male, Middle Aged, Prognosis, Prospective Studies, Renal Insufficiency, Chronic epidemiology, Risk Factors, Spain epidemiology, Acute Kidney Injury complications, Liver Cirrhosis complications, Patient Readmission, Renal Insufficiency, Chronic etiology, Severity of Illness Index
- Abstract
Background & Aims: Acute kidney injury (AKI) is common in cirrhosis and is associated with poor prognosis. In patients who survive after AKI, it is not known whether the acute injury leads to chronic impairment of kidney function (chronic kidney disease [CKD]). The aim of the study was to determine the frequency of CKD at 3 months after an AKI episode and its effects on patient outcomes., Methods: Patients admitted for complications of cirrhosis during a 6.5-year period were evaluated using the same protocol, with assessment of kidney function at regular intervals during and after hospitalization. CKD was defined as estimated glomerular filtration rate (eGFR) <60 ml/min/1.73m
2 at 3 months after AKI., Results: A total of 409 patients (168 with AKI and 241 without AKI) were included. After 3 months, 97 patients with AKI and 188 patients without AKI had survived. Of the 97 patients with AKI, 24 had developed CKD at 3 months compared to only 2 of the 188 patients without AKI (25% vs. 1%, odds ratio 31; p <0.0001). Risk factors independently associated with CKD were nosocomial AKI and severity of AKI (stage ≥1B). At diagnosis of CKD, all patients had stage 3A CKD and one-quarter of them progressed to stages 3B and 4 after 1 year. The transition from AKI to CKD was associated with an increased rate of 3-month hospital readmission, increased frequency of AKI, bacterial infections, ascites, and refractory ascites and a trend towards a higher need for liver transplantation. Transplant-free survival was not impaired., Conclusions: CKD frequently develops in patients with cirrhosis who survive AKI and has a negative impact on relevant clinical outcomes. The transition from AKI to CKD is common and should be considered a high-risk condition in patients with cirrhosis., Lay Summary: Episodes of acute impairment of kidney function are common in patients with cirrhosis. This study shows that the development of chronic impairment of kidney function is frequent in patients surviving these acute episodes and that it is associated with a higher risk of developing other complications of cirrhosis and to a higher rate of 3-month hospital readmissions., Competing Interests: Conflicts of interest PG reports Investigator Research grant and Advisory Board work from Grífols, Investigator Research grant and Advisory Board from Gilead, Investigator Research grant from Mallinckrodt, Advisory Board for Promethera, Advisory Board for Martin-Pharmaceuticals, grants from Ferring Pharmaceuticals, grants and Advisory Board Work from Sequana, outside the submitted work. The other authors have declared no conflict of interests. Please refer to the accompanying ICMJE disclosure forms for further details., (Copyright © 2020 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)- Published
- 2020
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6. Management of haemostatic alterations and associated disorders in cirrhosis in Spain: A national survey.
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Fortea JI, Puente Á, Ezcurra I, Cuadrado A, Arias-Loste MT, Cabezas J, Llerena S, Iruzubieta P, Rodríguez-Lope C, Huelin P, Casafont F, Fábrega E, and Crespo J
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- Adult, Blood Coagulation Disorders etiology, Female, Gastroenterology methods, Health Knowledge, Attitudes, Practice, Humans, International Normalized Ratio, Liver Cirrhosis therapy, Male, Middle Aged, Practice Guidelines as Topic, Risk Factors, Spain, Surveys and Questionnaires, Anticoagulants therapeutic use, Blood Coagulation Disorders drug therapy, Hemostasis physiology, Liver Cirrhosis complications, Practice Patterns, Physicians' statistics & numerical data
- Abstract
Background: Knowledge of haematological abnormalities in cirrhosis has greatly improved in recent years., Aims: To evaluate how Spanish Digestive Disease specialists manage haemostatic alterations and associated disorders in patients with cirrhosis., Methods: All members of the Spanish Association for the Study of the Liver and Spanish Society of Digestive Pathology were invited to fill in a web-based questionnaire., Results: 135 professionals, 93 hepatologists and 42 non-hepatologists responded to the survey. The concept of rebalanced haemostasis was known by 74.8% of them. Most specialists corrected the INR and thrombocytopenia before invasive procedures with moderate risk of bleeding or major surgery and in severe gastrointestinal bleeding. The threshold of platelets and, especially, INR used to administer blood products varied greatly. Pharmacological prophylaxis of venous thromboembolism prevailed, but it was highly dependent on the INR and platelet figures. Most participants initiated anticoagulation regardless of the degree of portal vein thrombosis, even in patients ineligible for transplantation. In potential candidates, only 56% maintained it indefinitely or until liver transplantation. No major differences between hepatologists and non-hepatologists were found., Conclusions: A significant variability and certain deviation from current guidelines was observed among Spanish Digestive Disease specialists regarding management of haemostatic alterations and associated disorders in cirrhosis., (Copyright © 2018 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.)
- Published
- 2019
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7. Midodrine and albumin for prevention of complications in patients with cirrhosis awaiting liver transplantation. A randomized placebo-controlled trial.
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Solà E, Solé C, Simón-Talero M, Martín-Llahí M, Castellote J, Garcia-Martínez R, Moreira R, Torrens M, Márquez F, Fabrellas N, de Prada G, Huelin P, Lopez Benaiges E, Ventura M, Manríquez M, Nazar A, Ariza X, Suñé P, Graupera I, Pose E, Colmenero J, Pavesi M, Guevara M, Navasa M, Xiol X, Córdoba J, Vargas V, and Ginès P
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- Adult, Aged, Albumins administration & dosage, Aldosterone blood, Ascites, Double-Blind Method, Female, Follow-Up Studies, Humans, Hyponatremia etiology, Hyponatremia prevention & control, Kaplan-Meier Estimate, Liver Cirrhosis mortality, Male, Middle Aged, Midodrine administration & dosage, Norepinephrine blood, Renal Insufficiency etiology, Renal Insufficiency prevention & control, Renin blood, Treatment Outcome, Vasoconstrictor Agents administration & dosage, Albumins therapeutic use, Liver Cirrhosis complications, Liver Cirrhosis drug therapy, Liver Transplantation, Midodrine therapeutic use, Shock prevention & control, Vasoconstrictor Agents therapeutic use
- Abstract
Background & Aims: Patients with decompensated cirrhosis on the waiting list for liver transplantation (LT) commonly develop complications that may preclude them from reaching LT. Circulatory dysfunction leading to effective arterial hypovolemia and activation of vasoconstrictor systems is a key factor in the pathophysiology of complications of cirrhosis. The aim of this study was to investigate whether treatment with midodrine, an alpha-adrenergic vasoconstrictor, together with intravenous albumin improves circulatory dysfunction and prevents complications of cirrhosis in patients awaiting LT., Methods: A multicenter, randomized, double-blind, placebo-controlled trial (NCT00839358) was conducted, including 196 consecutive patients with cirrhosis and ascites awaiting LT. Patients were randomly assigned to receive midodrine (15-30 mg/day) and albumin (40 g/15 days) or matching placebos for one year, until LT or drop-off from inclusion on the waiting list. The primary endpoint was incidence of any complication (renal failure, hyponatremia, infections, hepatic encephalopathy or gastrointestinal bleeding). Secondary endpoints were mortality, activity of endogenous vasoconstrictor systems and plasma cytokine levels., Results: There were no significant differences between both groups in the probability of developing complications of cirrhosis during follow-up (p = 0.402) or one-year mortality (p = 0.527). Treatment with midodrine and albumin was associated with a slight but significant decrease in plasma renin activity and aldosterone compared to placebo (renin -4.3 vs. 0.1 ng/ml.h, p < 0.001; aldosterone -38 vs. 6 ng/dl, p = 0.02, at week 48 vs. baseline). Plasma norepinephrine only decreased slightly at week 4. Neither arterial pressure nor plasma cytokine levels changed significantly., Conclusions: In patients with cirrhosis awaiting LT, treatment with midodrine and albumin, at the doses used in this study, slightly suppressed the activity of vasoconstrictor systems, but did not prevent complications of cirrhosis or improve survival., Lay Summary: Patients with cirrhosis who are on the liver transplant waiting list often develop complications which prevent them from receiving a transplant. Circulatory dysfunction is a key factor behind a number of complications. This study was aimed at investigating whether treating patients with midodrine (a vasoconstrictor) and albumin would improve circulatory dysfunction and prevent complications. This combined treatment, at least at the doses administered in this study, did not prevent the complications of cirrhosis or improve the survival of these patients., (Copyright © 2018 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)
- Published
- 2018
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8. Plasma copeptin as biomarker of disease progression and prognosis in cirrhosis.
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Solà E, Kerbert AJ, Verspaget HW, Moreira R, Pose E, Ruiz P, Cela R, Morales-Ruiz M, López E, Graupera I, Solé C, Huelin P, Navarro AA, Ariza X, Jalan R, Fabrellas N, Benten D, de Prada G, Durand F, Jimenez W, van der Reijden JJ, Fernandez J, van Hoek B, Coenraad MJ, and Ginès P
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- Biomarkers, Disease Progression, Glycopeptides, Humans, Prognosis, Prospective Studies, Liver Cirrhosis
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Background & Aims: Research on vasopressin (AVP) in cirrhosis and its role in the assessment of prognosis has been hindered by the difficulty of measuring AVP levels accurately. Copeptin, a 39-aminoacid glycopeptide, is released from the neurohypophysis together with AVP. Copeptin could have a role as biomarker of prognosis in cirrhosis as it may reflect circulatory dysfunction. The aim of this study is to investigate the role of copeptin as biomarker of disease progression and prognosis in cirrhosis., Methods: This prospective study is divided in 2 study protocols including 321 consecutive patients. Plasma copeptin levels were measured in all patients at study inclusion. Protocol 1: to investigate the relationship of copeptin with kidney and circulatory function (56 patients). Protocol 2: to investigate the relationship between copeptin and prognosis, as assessed by the development of complications of cirrhosis or mortality at 3months (265 patients admitted to hospital for complications of cirrhosis)., Results: Patients with decompensated cirrhosis showed significantly higher plasma copeptin levels compared to those of patients with compensated cirrhosis. Copeptin levels had a significant positive correlation with model for end-satge liver disease (MELD) score, AVP, endogenous vasoconstrictor systems, and kidney function parameters. Patients developing complications of cirrhosis or mortality had significantly higher plasma copeptin levels compared to those of the remaining patients. Plasma copeptin levels were an independent predictive factor of both the development of complications and mortality at 3months. This was confirmed in a validation series of 120 patients., Conclusions: Copeptin is a novel biomarker of disease progression and prognosis in cirrhosis., Lay Summary: Copeptin is a fragment of the vasopressin precursor, a hormone that is known to be increased in patients with cirrhosis and that plays a role in the development of complications of the disease. Vasopressin is difficult to measure, but copeptin is a more stable molecule and is easier to measure in blood. Solà and Kerbert and colleagues have shown in a series of 361 patients that copeptin is markedly increased in patients with cirrhosis who develop complications during the following 3months, compared to those patients who do not develop complications. Moreover, copeptin correlates with prognosis., (Copyright © 2016 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)
- Published
- 2016
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9. Neutrophil gelatinase-associated lipocalin is a biomarker of acute-on-chronic liver failure and prognosis in cirrhosis.
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Ariza X, Graupera I, Coll M, Solà E, Barreto R, García E, Moreira R, Elia C, Morales-Ruiz M, Llopis M, Huelin P, Solé C, Fabrellas N, Weiss E, Nevens F, Gerbes A, Trebicka J, Saliba F, Fondevila C, Hernández-Gea V, Fernández J, Bernardi M, Arroyo V, Jiménez W, Deulofeu C, Pavesi M, Angeli P, Jalan R, Moreau R, Sancho-Bru P, and Ginès P
- Subjects
- Acute Kidney Injury, Biomarkers, Humans, Lipocalin-2, Liver Cirrhosis, Prognosis, Acute-On-Chronic Liver Failure
- Abstract
Background & Aims: Acute-on-chronic liver failure (ACLF) is a syndrome that occurs in cirrhosis characterized by organ failure(s) and high mortality rate. There are no biomarkers of ACLF. The LCN2 gene and its product, neutrophil gelatinase-associated lipocalin (NGAL), are upregulated in experimental models of liver injury and cultured hepatocytes as a result of injury by toxins or proinflammatory cytokines, particularly Interleukin-6. The aim of this study was to investigate whether NGAL could be a biomarker of ACLF and whether LCN2 gene may be upregulated in the liver in ACLF., Methods: We analyzed urine and plasma NGAL levels in 716 patients hospitalized for complications of cirrhosis, 148 with ACLF. LCN2 expression was assessed in liver biopsies from 29 additional patients with decompensated cirrhosis with and without ACLF., Results: Urine NGAL was markedly increased in ACLF vs. no ACLF patients (108(35-400) vs. 29(12-73)μg/g creatinine; p<0.001) and was an independent predictive factor of ACLF; the independent association persisted after adjustment for kidney function or exclusion of variables present in ACLF definition. Urine NGAL was also an independent predictive factor of 28day transplant-free mortality together with MELD score and leukocyte count (AUROC 0.88(0.83-0.92)). Urine NGAL improved significantly the accuracy of MELD in predicting prognosis. The LCN2 gene was markedly upregulated in the liver of patients with ACLF. Gene expression correlated directly with serum bilirubin and INR (r=0.79; p<0.001 and r=0.67; p<0.001), MELD (r=0.68; p<0.001) and Interleukin-6 (r=0.65; p<0.001)., Conclusions: NGAL is a biomarker of ACLF and prognosis and correlates with liver failure and systemic inflammation. There is remarkable overexpression of LCN2 gene in the liver in ACLF syndrome., Lay Summary: Urine NGAL is a biomarker of acute-on-chronic liver failure (ACLF). NGAL is a protein that may be expressed in several tissues in response to injury. The protein is filtered by the kidneys due to its small size and can be measured in the urine. Ariza, Graupera and colleagues found in a series of 716 patients with cirrhosis that urine NGAL was markedly increased in patients with ACLF and correlated with prognosis. Moreover, gene coding NGAL was markedly overexpressed in the liver tissue in ACLF., (Copyright © 2016 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)
- Published
- 2016
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10. Severe acute kidney injury associated with non-steroidal anti-inflammatory drugs in cirrhosis: A case-control study.
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Elia C, Graupera I, Barreto R, Solà E, Moreira R, Huelin P, Ariza X, Solé C, Pose E, Baiges A, Fabrellas N, Poch E, Fernández J, Arroyo V, and Ginès P
- Subjects
- Acute Kidney Injury mortality, Acute-Phase Proteins urine, Adult, Aged, Case-Control Studies, Cohort Studies, Female, Humans, Lipocalin-2, Lipocalins urine, Male, Middle Aged, Prospective Studies, Proto-Oncogene Proteins urine, Acute Kidney Injury chemically induced, Anti-Inflammatory Agents, Non-Steroidal adverse effects, Liver Cirrhosis drug therapy
- Abstract
Background & Aims: Non-steroidal anti-inflammatory drugs (NSAIDs) may cause impairment of kidney function in patients with cirrhosis. Investigational studies demonstrated reversibility of kidney dysfunction after drug withdrawal, but information based on clinical practice is lacking. The aim of the study was to investigate the characteristics and outcome of Acute Kidney Injury (AKI) developing in patients with cirrhosis treated with NSAIDs., Methods: Prospective cohort study in a tertiary referral center of all patients with NSAIDs-associated AKI seen from 2002 to 2014. For comparison, three control groups of patients with hypovolemic-induced AKI, type-1 HRS and ATN, respectively, were also evaluated. Urinary excretion of neutrophil gelatinase-associated lipocalin (uNGAL) was measured in a subset of patients., Results: Thirty patients with cirrhosis and NSAIDs-associated AKI were identified. In 19 patients (63%) AKI was transient and kidney function rapidly recovered (4±3 days) after NSAIDs withdrawal. In the remaining 11 patients (37%) AKI was more severe and persisted during hospitalization despite drug withdrawal. Patients with persistent AKI had remarkably higher uNGAL levels compared with those of patients with transient AKI (953±1,198 vs. 83±79 μg/g of creatinine, respectively, p=0.008). Moreover, seven of the 11 patients with persistent AKI (64%) died within three months compared with only one of the 19 (5%) patients with transient AKI (p=0.001). Mortality of persistent AKI was similar in NSAIDs patients compared to control groups. The only independent predictive factor of three-month mortality was persistent AKI., Conclusions: Patients with cirrhosis treated with NSAIDs may develop severe AKI which may be irreversible and associated with poor short-term outcome., (Copyright © 2015 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)
- Published
- 2015
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