Hepatitis C virus: the nephrologist's view.

The last 4 years have been a period of rapid expansion in our understanding of both the molecular biology and clinical significance of hepatitis C virus (HCV) infection. Initial studies using first-generation enzyme-linked immunosorbent assays suggested that the end-stage renal disease population had an exceptionally high prevalence of anti-HCV compared with asymptomatic healthy blood donors. Subsequent analyses with second-generation assays and polymerase chain reaction techniques to detect viremia confirmed these earlier studies. Considering the prevalence of HCV within the dialysis population, it comes as no surprise that several studies confirmed HCV as the leading cause of non-A, non-B hepatitis among renal allograft recipients. Furthermore, transmission of HCV by transplantation of a kidney from an HCV-infected organ donor has been unequivocally demonstrated. The natural history of HCV infection in the immunosuppressed allograft recipient and its impact on long-term patient outcome are still being analyzed. Finally, HCV has been associated with essential mixed cryoglobulinemia and several histologic patterns of immune complex glomerulonephritis, including membranous and membrano-proliferative glomerulonephritis. Although HCV antigen-antibody complexes have not been demonstrated in the kidney, the marked decrease in proteinuria following clearance of HCV RNA with interferon alpha-2b therapy suggests an etiologic role for HCV in these glomerular diseases. Furthermore, the demonstration of HCV RNA in the cryoprecipitate of patients with essential mixed cryoglobulinemia and a beneficial response to treatment with interferon alpha-2b also suggest a role for HCV in the pathogenesis of these clinical syndromes.