Treatment of hepatitis C in kidney transplant recipients with interferon alpha-2b plus ribavirin

Abstract

Session B. Clinical Nephrology - B7. Hepatitis in glomerular disease, dialysis and transplant patientsLimited data is available for the treatment of hepatitis C virus (HCV) infection in renal allograft recipients, in whom interferon therapy is generally regarded as contraindicated due to potential risks of acute rejection or graft dysfunction. We treated 4 patients who acquired acute hepatitis C in the perioperative period of kidney transplantation. All four patients, who were not HCV carriers before renal transplantation, developed acute transaminitis with negative anti-HCV serology, but positive circulating HCV RNA detectable by PCR. All patients were on cyclosporin-based immunosuppressive protocol. They received interferon alpha-2b (3 MU s.c. thrice weekly) and ribavirin (800-1200 mg p.o. daily according to body weight and hemoglobin levels) treatment. As shown in Table 1, three patients had complete remission with normalization of serum alanine aminotransferase (ALT) level within 4-12 weeks of therapy, and disappearance of serum HCV RNA at 24 and 48 weeks of starting therapy. Two of them had persistently undetectable HCV RNA at 24 weeks after cessation of therapy, while one had just completed the 48-week treatment at the time of writing. The non-responder, in whom treatment was stopped after 24 weeks due to persistent HCV-viremia, was infected with HCV gentotype 1b, which is known to be associated with a less favorable treatment response. All patients had stable renal allograft function throughout the course of treatment. Ribavirin-induced hemolysis, which was dose-dependent, was the most common side-effect. We conclude that combination interferon/ribavirin therapy can be a valid therapeutic option in renal transplant recipients with hepatitis C, but the decision on treatment should take into consideration the severity, progression, and prognosis of the hepatitis, the potential efficacy based on the HCV genotype, and the risk of inducing allograft dysfunction.Link_to_subscribed_fulltex