title: A 20-year case study of a kidney transplant recipient with chronic active hepatitis C: clinical course and successful treatment for late acute rejection induced by interferon therapy.
abstract: BACKGROUND
  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)-alpha therapy; and the risk of IFN-alpha therapy.
  
  
  METHODS
  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.
  
  
  RESULTS
  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 post-transplant year and HCV genome was detected in the 17th year. IFN-alpha 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.
  
  
  CONCLUSIONS
  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-alpha could induce acute cellular rejection even in the 17th year. Such acute rejection can be reversible with OKT3.
authors.affiliation: Department of Urology, Kidney Transplant Center, Hyogo Prefectural Nishinomiya Hospital, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Ichikawa
authors.forename: M
authors.initials: M
authors.lastname: Kyo
authors.forename: T
authors.initials: T
authors.lastname: Hanafusa
authors.forename: T
authors.initials: T
authors.lastname: Kohro
authors.forename: H
authors.initials: H
authors.lastname: Kishikawa
authors.forename: T
authors.initials: T
authors.lastname: Fukunishi
authors.forename: S
authors.initials: S
authors.lastname: Nagano
authors.forename: Y
authors.initials: Y
authors.lastname: Shinji
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use; D005500:Follow-Up Studies; D016174:Hepacivirus / Q000276:immunology / Q000502:physiology; D018937:Hepatitis C Antibodies / Q000032:analysis; D019698:Hepatitis C, Chronic / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use; D016030:Kidney Transplantation / Q000473:pathology; D008099:Liver / Q000473:pathology; D008297:Male; D011183:Postoperative Complications; D017735:Virus Latency
chemical_list: D000998:Antiviral Agents; D018937:Hepatitis C Antibodies; D016898:Interferon-alpha