Hepatitis C Virus Infection in Chronic Kidney Disease

Abstract

Soon after the hepatitis C virus (HCV) was identified in 1989, it was recognized that the prevalence of infection in patients with ESRD far exceeded that in the general population. Infection with HCV predisposes to the hepatic complications of cirrhosis and hepatocellular carcinoma. However, important extrahepatic manifestations include immune complex glomerular disease, accelerated progression of CKD, increases in cardiovascular event risk, and lymphoproliferative disorders. Advances in understanding the molecular biology of HCV have ushered in a new era in the treatment of this infection. Second generation direct-acting antiviral agents have revolutionized therapy, with sustained virologic response rates (undetectable viral load 12 weeks after completing therapy) of >90% in most patients. Studies using direct-acting antivirals in patients with CKD and those on dialysis are showing excellent safety and efficacy as well. In this context, it is imperative that nephrologists become familiar with this literature, reviewed here, so that the important decisions, including which patients should be treated and the optimal timing to initiate therapy, are vetted in association with the compounding issues of CKD, ESRD, and kidney transplantation.

Keywords: chronic kidney disease; hepatitis; kidney transplantation.

Figure 1.

The HCV genome and target sites of action for the direct acting antiviral agents. Combining agents with different mechanisms of viral interference has resulted in the achievement of very high sustained viral response rates. NTR, nontranslated region.

Figure 2.

Suggested paradigm for the management of the HCV-infected pretransplant candidate. Critical decision points include whether the patient has a living donor and the extent of liver fibrosis. The option to accept a kidney from a HCV positive donor could significantly shorten wait times. HVPG, hepatic venous pressure gradient; Neg, negative; Pos, positive; SVR, sustained virologic response; DAA, direct antiviral agent.