title: The long-term course of hepatitis C after kidney transplantation.
abstract: Patients with chronic hepatitis run the risk of developing progressive liver disease during immunosuppressive therapy after kidney transplantation. To determine the impact of chronic hepatitis C on morbidity and mortality we analyzed 162 anti-HCV positive of 1241 renal-grafted patients (prevalence 13.1%; 84.9% HCV RNA positive) regularly surveyed in our outpatient clinic between 1992 and 1994. The mean age at transplantation was 44.5 (6-69) years, and follow-up after grafting was 7.4 (0.1-23.9) years. The immunosuppressive regimen and frequency of rejection episodes in HCV-infected patients were comparable to the total population. Only 4.3% (5/117) of the anti-HCV positive, HBV negative patients living with functioning grafts developed a markedly compromised liver function. Fifteen (9.3%) of the HCV-infected patients died, but none suffered from posthepatitic cirrhosis. An additional retrospective analysis of causes of death after transplantation prior to 1992 revealed that liver disease had only been responsible for 2% of the deaths (7 of 324) in the HBsAg negative population (n= 1901). In contrast, the predominant cause of death in the HBsAg positive population (n=76) was posthepatitic cirrhosis in 58% (15 of 26). Thus, kidney transplantation in patients with replicative hepatitis C and normal liver function appears to be justified because of low early and late morbidity and mortality due to chronic liver disease. HBV infection and hemosiderosis substantially increase the risk of chronic liver disease in renal transplant recipients with hepatitis C.
authors.affiliation: Abteilung Nephrologie, Medizinische Hochschule Hannover, Germany.
authors.forename: V
authors.initials: V
authors.lastname: Kliem
authors.forename: U
authors.initials: U
authors.lastname: van den Hoff
authors.forename: R
authors.initials: R
authors.lastname: Brunkhorst
authors.forename: H L
authors.initials: HL
authors.lastname: Tillmann
authors.forename: J
authors.initials: J
authors.lastname: Flik
authors.forename: M P
authors.initials: MP
authors.lastname: Manns
authors.forename: R
authors.initials: R
authors.lastname: Pichlmayr
authors.forename: K M
authors.initials: KM
authors.lastname: Koch
authors.forename: U
authors.initials: U
authors.lastname: Frei
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000961:Antilymphocyte Serum / Q000627:therapeutic use; D002648:Child; D016572:Cyclosporine / Q000627:therapeutic use; D005260:Female; D006084:Graft Rejection / Q000628:therapy; D006486:Hemosiderosis / Q000150:complications; D006509:Hepatitis B / Q000150:complications; D006514:Hepatitis B Surface Antigens / Q000032:analysis; D006526:Hepatitis C / Q000453:epidemiology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D016030:Kidney Transplantation / Q000009:adverse effects* / Q000276:immunology; D008099:Liver / Q000201:enzymology / Q000502:physiology; D008297:Male; D008775:Methylprednisolone / Q000627:therapeutic use; D008875:Middle Aged; D016853:Muromonab-CD3 / Q000627:therapeutic use; D011239:Prednisolone / Q000627:therapeutic use; D015995:Prevalence; D012189:Retrospective Studies; D016896:Treatment Outcome
chemical_list: D000961:Antilymphocyte Serum; D006514:Hepatitis B Surface Antigens; D007166:Immunosuppressive Agents; D016853:Muromonab-CD3; D016572:Cyclosporine; D011239:Prednisolone; D008775:Methylprednisolone