A 20-YEAR CASE STUDY OF A KIDNEY TRANSPLANT RECIPIENT WITH CHRONIC ACTIVE HEPATITIS C

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Abstract
The influence of hepatitis C virus (HCV) infection has been discussed in kidney transplantation. Our case study focused on four points: the clinical course of an HCV-infected recipient; the pathogenesis of hepatic disorders in such a patient; interferon (IFN)-α therapy; and the risk of IFN-α therapy. A patient was suspected of acquiring HCV via transfusion at kidney transplant. He was examined several times serologically, virologically, endoscopically, and pathologically during a 20-year follow-up. Abnormal biochemical markers were found within a month after transplantation but recovery occurred without any treatment. Within 3 years postoperatively, hepatic disorder developed including peliosis hepatis, nodular regenerative hyperplasia, and cholestasis. These pathological conditions were ascribed to immunosuppressants: cyclophosphamide and azathioprine. Abnormal chemical markers decreased to normal values for 4 consecutive years with the substitution of cyclophosphamide and azathioprine for mizoribine. During the subsequent 13 years, the patient developed chronic hepatitis with clinical and morphological features of hepatitis C infection. Anti-HCV antibody was positive from the second posttransplant year and HCV genome was detected in the 17th year. IFN-α therapy was initiated in the 17th year and resulted in normal transaminase activities with no effect on viremia. However, acute cellular rejection developed. The rejection was steroid resistant but responsive to OKT3. HCV might remain latent for approximately 7 years even in kidney recipients unless toxic hepatitis occurs. Hepatotoxic drugs may cause a wide spectrum of liver diseases in HCV carriers as a result of the overload of immunosuppressants on hepatocytes. IFN-α could induce acute cellular rejection even in the 17th year. Such acute rejection can be reversible with OKT3.