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Hepatitis C virus infection and renal transplantation

INTRODUCTION

Liver disease is an important cause of morbidity and mortality among recipients of transplanted organs. Biochemical abnormalities in liver function are seen in 7 to 24 percent of transplant recipients, and liver failure is the cause of death in 8 to 28 percent of long-term survivors after renal transplantation [1,2].

Previously, approximately one-half of the cases of liver disease among transplanted patients were attributed to a variety of etiologies, including viral infections such as hepatitis B virus (HBV), Epstein-Barr virus, or cytomegalovirus (CMV); drugs such as azathioprine or cyclosporine; hemosiderosis; or alcohol. The remaining one-half of cases were attributed to non-A, non-B hepatitis (NANBH) [3-5].

The cloning and characterization of hepatitis C virus (HCV) has permitted the development and refinement of tests to detect antibodies to multiple HCV antigens (anti-HCV) and the presence and titer of HCV RNA. These modalities have opened avenues to the study of the prevalence, transmission, and natural course of HCV infection in transplant recipients.

The clinical issues relating to HCV infection in renal transplantation are presented here. The role of HCV in causing renal disease in transplant recipients is discussed separately. (See "Renal disease associated with hepatitis C virus after renal transplantation".)

HEPATITIS C VIRUS AND TRANSPLANTATION

Studies have focused attention upon the extremely high rate of transmitted infection and the significant morbidity and mortality associated with hepatitis C virus (HCV) in the immunosuppressed transplant recipient [6-8]. This has forced national and international organ banks to examine their policies concerning transplantation in the patient infected with HCV and the allocation of organs from HCV-positive or negative donors into HCV-positive or negative recipients.

               

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Literature review current through: Sep 2014. | This topic last updated: Aug 15, 2014.
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