Hepatitis C virus viremia increases the incidence of chronic kidney disease in HIV-infected patients.
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 1.73 m or less for patients with a baseline eGFR more than 60 ml/min per 1.73 m or a confirmed 25% decline in eGFR for patients with a baseline eGFR of 60 ml/min per 1.73 m 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-HCV-positive of whom 983 (47.9%) were HCV-RNA-positive, 193 (9.4%) HCV-RNA-negative 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 1.73 m. During 36123 person-years 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.


CONCLUSIONS
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.
Copenhagen HIV Programme, University of Copenhagen, Copenhagen, Denmark. lpe@cphiv.dk
Lars
L
Peters
Daniel
D
Grint
Jens D
JD
Lundgren
Jürgen K
JK
Rockstroh
Vincent
V
Soriano
Peter
P
Reiss
Anna
A
Grzeszczuk
Helen
H
Sambatakou
Amanda
A
Mocroft
Ole
O
Kirk
D016263:AIDS-Associated Nephropathy / Q000453:epidemiology* / Q000276:immunology; D000328:Adult; D001118:Argentina / Q000453:epidemiology; D015331:Cohort Studies; D003404:Creatinine / Q000097:blood; D018450:Disease Progression; D005060:Europe / Q000453:epidemiology; D005260:Female; D005838:Genotype; D005919:Glomerular Filtration Rate; D006679:HIV Seropositivity / Q000150:complications* / Q000453:epidemiology / Q000276:immunology; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology*; D006526:Hepatitis C / Q000150:complications* / Q000453:epidemiology / Q000276:immunology; D018937:Hepatitis C Antibodies / Q000235:genetics / Q000276:immunology*; D006801:Humans; D015994:Incidence; D007557:Israel / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D051436:Renal Insufficiency, Chronic / Q000453:epidemiology* / Q000276:immunology / Q000821:virology*; D014766:Viremia / Q000150:complications* / Q000821:virology
D018937:Hepatitis C Antibodies; D003404:Creatinine