Hepatitis C and renal disease: epidemiology, diagnosis, pathogenesis and therapy

Abstract

There is an increased evidence for the association between hepatitis C virus (HCV) infection and kidney diseases. Recent epidemiological studies strongly suggest that HCV infection is a risk factor for proteinuria and/or impaired renal function. Type I membranoproliferative glomerulonephritis (MPGN) associated with type II cryoglobulinemia is the most frequent renal disease, and non-cryoglobulinemic MPGN and membranous glomerulonephritis are less frequently associated with active HCV infection. The pathogenesis of these lesions are related to the deposition of immune complexes in the glomeruli, and recently it has been described that toll-like receptor 3 could have a pathogenic role establishing a link between viral infection and glomerulonephritis. Patients with HCV-related glomerulopathies should be treated with angiotensin-converting enzyme inhibitors in association or not with angiotensin receptor blockers, as well as with anti-HCV therapy. The latter relies on a combined antiviral therapy of standard or pegylated interferon-α and ribavirin. We recommend the treatment of patients for at least 48 weeks, and the continuation of antiviral therapy, even in the absence of a decrease in HCV RNA concentration of 2-log at week 12. Ribavirin doses should be adapted according to creatinine clearance in order to avoid its main side effect, i.e. hemolytic anemia. Combined antiviral therapy and immunosuppression (cyclophosphamide or rituximab with steroids) may be the treatment of choice for patients with severe renal disease, i.e. nephrotic syndrome and/or progressive renal failure, or diseases that are refractory to anti-HCV therapy alone.