Liver dysfunction is a major cause of morbidity and mortality in patients receiving renal transplantation. We clinically studied on the posttransplant liver dysfunction in 332 renal allograft recipients at our institute during the past 20 years. The result showed that the incidence of post-transplant liver dysfunction was 16.9% (56/332). Among 56 patients drug-induced liver dysfunction accounted for 75% (42/56), while viral infection such as hepatitis B and C viruses (HBV and HCV, respectively), or cytomegalovirus was responsible for liver dysfunction in 10 other patients. Drug-induced liver dysfunction occurred within 30 days following renal transplantation in most patients. The duration of abnormality in the serum transaminase was significantly shorter in drug-induced liver dysfunction than in virus-related one. With respect to HCV-related liver dysfunction, in 67 patients who were measured for the second generation anti-HCS: antibody, thirteen (19.4%) were positive for anti-HCV antibody. Among them 6 patients (46.2%) showed long-lasting abnormality in the serum transaminase, though the patients did not have any impaired grafts' function with graft survival being more than 10 years. The quantitative HCV-RNA analysis further demonstrated that the titers of HCV RNA were higher than 1 Meq/ml in all patients with chronic liver dysfunction who were positive for anti-HCV antibody. The HCV genotype in the patients was type 2, According to recent reports the interferon therapy for HCV may be less efficacious in patients with the I-ICS' genotype 2. In immunocompetent patients, persistent HCV infection is associated with the development of chronic active hepatitis that may, at times, result in liver cirrhosis and/or hepatocellular carcinoma. A close follow up after renal transplantation is, thus, required for in the posttransplant patients with anti-HCV antibody.
