Association of hepatitis C virus infection with prevalence and development of kidney disease.

BACKGROUND: Hepatitis C and chronic kidney disease (CKD) are both highly prevalent diseases in the United States. Data showed that hepatitis C may be causally linked to some glomerular diseases, and patients who are positive for hepatitis C have increased risk of albuminuria. STUDY
DESIGN: To determine whether hepatitis C infection is associated with increased likelihood of CKD, we performed retrospective cross-sectional and longitudinal analyses of a large clinical database. SETTING & PARTICIPANTS: Data for a study population of 13,139 African American and white patients tested for hepatitis C between 1994 and 2004 were extracted from a computerized database from a clinical population of an urban hospital and affiliated clinics. PREDICTOR: Hepatitis C by means of enzyme-linked immunosorbent assay. OUTCOME: In cross-sectional analysis, CKD was defined as a minimum estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m(2) by using the 4-variable isotope dilution mass spectrometry-traceable Modification of Diet in Renal Disease Study equation or proteinuria. In longitudinal analysis, CKD was defined as eGFR less than 60 mL/min/1.73 m(2). MEASUREMENTS: Potential confounders investigated included sex, age, race, human immunodeficiency virus (HIV) status, chronic hypertension, diabetes, and other laboratory test result abnormalities.
RESULTS: 3,938 patients (30.0%) were positive for hepatitis C and 2,549 (19.4%) had CKD. Of those with CKD, 1,999 (78.4%) had an eGFR less than 60 mL/min/1.73 m(2), 186 (7.3%) had proteinuria, and 364 (14.3%) had both. In cross-sectional analysis, after controlling for diabetes, hypertension, age, aspartate aminotransferase level, and HIV status, patients who tested positive for hepatitis C had a decreased risk of CKD (odds ratio, 0.69; 95% confidence interval, 0.62 to 0.77). A total of 7,038 subjects without CKD were followed up for a median of 3.5 years. Of these, 2,243 (31.8%) were hepatitis C positive at the onset of follow-up. In longitudinal analysis, after adjustment for age, baseline eGFR, diabetes, hypertension, aspartate aminotransferase level, and HIV status, the hazard ratio for the development of CKD compared with those who were hepatitis C negative was 0.896 (95% confidence interval, 0.790 to 1.015). LIMITATIONS: Retrospective design, clinical database with missing values, different hepatitis C assays used during the study period, limited data for proteinuria.
CONCLUSIONS: Our results do not support the hypothesis that infection with hepatitis C virus per se is associated with increased risk of having or developing CKD.