Background: Several studies have reported on an association between hepatitis C virus (HCV) antibody status and the development of chronic kidney disease (CKD), but the role of HCV viremia and genotype are not well defined. Methods: Patients with at least three serum creatinine measurements after 1 January 2004 and known HCV antibody status were included. Baseline was defined as the first eligible estimated glomerular filtration rate (eGFR) (Cockcroft-Gault equation), and CKD was either a confirmed (>3 months apart) eGFR of 60 ml/min per 1.73m2 or less for patients with a baseline eGFR more than 60 ml/min per 1.73m2 or a confirmed 25% decline in eGFR for patients with a baseline eGFR of 60 ml/min per 1.73m2 or less. Incidence rates of CKD were compared between HCV groups (anti-HCV-negative, anti-HCV-positive with or without viremia) using Poisson regression. Results: Of 8235 patients with known anti-HCV status, 2052 (24.9%) were anti-HCVpositive of whom 983 (47.9%) were HCV-RNA-positive, 193 (9.4%) HCV-RNAnegative and 876 (42.7%) had unknown HCV-RNA. At baseline, the median eGFR was 97.6 (interquartile range 83.8-113.0) ml/min per 1.73m2. During 36123 personyears of follow-up (PYFU), 495 patients progressed to CKD (6.0%) with an incidence rate of 14.5 per 1000 PYFU (95% confidence interval 12.5-14.9). In a multivariate Poisson model, patients who were anti-HCV-positive with HCV viremia had a higher incidence rate of CKD, whereas patients with cleared HCV infection had a similar incidence rate of CKD compared with anti-HCV-negative patients. There was no association between CKD and HCV genotype. Conclusion: Compared with HIV-monoinfected patients, HIV-positive patients with chronic rather than cleared HCV infection were at increased risk of developing CKD, suggesting a contribution from active HCV infection toward the pathogenesis of CKD.

Hepatitis c virus viremia increases the Incidence of chronic kidney disease in HIV-infected Patients / L. Peters, D. Grint, J.D. Lundgren, J.K. Rockstroh, V. Soriano, P. Reiss, A. Grzeszczuk, H. Sambatakou, A. Mocroft, O. Kirk, M. Losso, C. Elias, N. Vetter, R. Zangerle, I. Karpov, A. Vassilenko, V.M. Mitsura, O. Suetnov, N. Clumeck, S. De Wit, M. Delforge, R. Colebunders, L. Vandekerckhove, V. Hadziosmanovic, K. Kostov, J. Begovac, L. Machala, D. Jilich, D. Sedlacek, J. Nielsen, G. Kronborg, T. Benfield, M. Larsen, J. Gerstoft, T. Katzenstein, A.-.E. Hansen, P. Skinhoj, C. Pedersen, L. Ostergaard, K. Zilmer, J. Smidt, M. Ristola, C. Katlama, J.-. Viard, P.-. Girard, J.M. Livrozet, P. Vanhems, C. Pradier, F. Dabis, D. Neau, R. Schmidt, J. Van Lunzen, O. Degen, H.J. Stellbrink, S. Staszewski, J. Bogner, G. Fatkenheuer, J. Kosmidis, P. Gargalianos, G. Xylomenos, J. Perdios, G. Panos, A. Filandras, E. Karabatsaki, D. Banhegyi, F. Mulcahy, I. Yust, D. Turner, M. Burke, S. Pollack, G. Hassoun, S. Maayan, S. Vella, R. Esposito, I. Mazeu, C. Mussini, C. Arici, R. Pristera, F. Mazzotta, A. Gabbuti, V. Vullo, M. Lichtner, A. Chirianni, E. Montesarchio, M. Gargiulo, G. Antonucci, A. Testa, P. Narciso, C. Vlassi, M. Zaccarelli, A. Lazzarin, A. Castagna, N. Gianotti, M. Galli, A. Ridolfo, A. D'Arminio Monforte, B. Rozentale, I. Zeltina, S. Chaplinskas, R. Hemmer, T. Staub, V. Ormaasen, A. Maeland, J. Bruun, B. Knysz, J. Gasiorowski, A. Horban, E. Bakowska, R. Flisiak, A. Boron-Kaczmarska, M. Pynka, M. Parczewski, M. Beniowski, E. Mularska, H. Trocha, E. Jablonowska, E. Malolepsza, K. Wojcik, F. Antunes, M. Doroana, L. Caldeira, K. Mansinho, F. Maltez, D. Duiculescu, V. Babes, A. Rakhmanova, N. Zakharova, S. Buzunova, D. Jevtovic, M. Mokras, D. Stanekova, J. Tomazic, J. Gonzalez-Lahoz, P. Labarga, J. Medrano, S. Moreno, J.M. Rodriguez, B. Clotet, A. Jou, R. Paredes, C. Tural, J. Puig, I. Bravo, J.M. Gatell, J.M. Miro, P. Domingo, M. Gutierrez, G. Mateo, M.A. Sambeat, A. Karlsson, L. Flamholc, B. Ledergerber, R. Weber, P. Francioli, M. Cavassini, B. Hirschel, E. Boffi, H. Furrer, M. Battegay, L. Elzi, E. Kravchenko, N. Chentsova, V. Frolov, G. Kutsyna, S. Servitskiy, M. Krasnov, S. Barton, A.M. Johnson, D. Mercey, A. Phillips, M.A. Johnson, M. Murphy, J. Weber, G. Scullard, M. Fisher, C. Leen. - In: AIDS. - ISSN 0269-9370. - 26:15(2012 Sep 24), pp. 1917-1926. [10.1097/QAD.0b013e3283574e71]

Hepatitis c virus viremia increases the Incidence of chronic kidney disease in HIV-infected Patients

M. Galli;A. D'Arminio Monforte;
2012

Abstract

Background: Several studies have reported on an association between hepatitis C virus (HCV) antibody status and the development of chronic kidney disease (CKD), but the role of HCV viremia and genotype are not well defined. Methods: Patients with at least three serum creatinine measurements after 1 January 2004 and known HCV antibody status were included. Baseline was defined as the first eligible estimated glomerular filtration rate (eGFR) (Cockcroft-Gault equation), and CKD was either a confirmed (>3 months apart) eGFR of 60 ml/min per 1.73m2 or less for patients with a baseline eGFR more than 60 ml/min per 1.73m2 or a confirmed 25% decline in eGFR for patients with a baseline eGFR of 60 ml/min per 1.73m2 or less. Incidence rates of CKD were compared between HCV groups (anti-HCV-negative, anti-HCV-positive with or without viremia) using Poisson regression. Results: Of 8235 patients with known anti-HCV status, 2052 (24.9%) were anti-HCVpositive of whom 983 (47.9%) were HCV-RNA-positive, 193 (9.4%) HCV-RNAnegative and 876 (42.7%) had unknown HCV-RNA. At baseline, the median eGFR was 97.6 (interquartile range 83.8-113.0) ml/min per 1.73m2. During 36123 personyears of follow-up (PYFU), 495 patients progressed to CKD (6.0%) with an incidence rate of 14.5 per 1000 PYFU (95% confidence interval 12.5-14.9). In a multivariate Poisson model, patients who were anti-HCV-positive with HCV viremia had a higher incidence rate of CKD, whereas patients with cleared HCV infection had a similar incidence rate of CKD compared with anti-HCV-negative patients. There was no association between CKD and HCV genotype. Conclusion: Compared with HIV-monoinfected patients, HIV-positive patients with chronic rather than cleared HCV infection were at increased risk of developing CKD, suggesting a contribution from active HCV infection toward the pathogenesis of CKD.
coinfection; hepatitis C virus; HIV; kidney disease; viremia; AIDS-Associated Nephropathy; Adult; Argentina; Cohort Studies; Creatinine; Disease Progression; Europe; Female; Genotype; Glomerular Filtration Rate; HIV Seropositivity; Hepacivirus; Hepatitis C; Hepatitis C Antibodies; Humans; Incidence; Israel; Male; Middle Aged; Prospective Studies; Renal Insufficiency, Chronic; Viremia
Settore MED/17 - Malattie Infettive
24-set-2012
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/774438
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