Indexed on: 31 Oct '01Published on: 31 Oct '01Published in: American Journal of Kidney Diseases
With the success of organ transplantation, liver disease has emerged as an important cause of morbidity and mortality of renal transplant (RT) recipients. Numerous studies performed during the 1990s have shown that hepatitis C virus (HCV) infection is the leading cause of chronic liver disease among RT recipients. The transmission of HCV by renal transplantation of a kidney from an HCV-infected organ donor has been shown unequivocally. Liver biopsy is essential in the evaluation of liver disease of RT recipients, and histological studies have shown that HCV-related liver disease after renal transplantation is progressive. The outcome of HCV-related liver disease is probably more aggressive in RT recipients than immunocompetent individuals. Various factors can affect the progression of HCV in the RT population: coinfection with hepatitis B virus, time of HCV acquisition, type of immunosuppressive treatment, and concomitant alcohol abuse. The role of virological features of HCV remains unclear. The natural history of HCV infection after renal transplantation is under evaluation; however, recent surveys with long follow-ups have documented adverse effects of HCV infection on patient and graft survival in RT recipients. Use of renal grafts from HCV-infected donors in recipients with HCV infection does not appear to result in a greater burden of liver disease, at least for a short period. The association between HCV and de novo or recurrent glomerulonephritis after RT has been hypothesized and is an area of avid research. Reported studies do not support interferon (IFN) treatment for RT recipients with chronic hepatitis C because of the frequent occurrence of graft failure, and information on the use of other types of IFN or combined therapy (IFN plus ribavirin or amantadine) is not yet available in the RT population.