title: Renal disease in hepatitis C-positive liver transplant recipients.
abstract: Glomerular abnormalities are frequent in patients undergoing liver transplantation; however, renal dysfunction following transplantation is mainly attributed to cyclosporine toxicity. Membranoproliferative glomerulonephritis (MPGN) is seen in patients infected with hepatitis C virus (HCV), the virus responsible for 30% of the end-stage liver disease leading to liver transplantation. To determine the incidence of renal abnormalities in liver transplant recipients and the association with HCV, we undertook a longitudinal study in HCV-positive (n=91) and HCV-negative (n=106) liver transplant recipients. Mean creatinine clearance before transplantation was 94 ml/min/1.73 m2 in HCV+ patients and 88 ml/min/1.73 m2 in HCV- patients. By 3 months after transplantation, the mean creatinine clearance decreased by approximately one third in both groups. A greater proportion of HCV+ patients excreted >2 g protein/day after transplantation (P=0.05) and had renal biopsies showing MPGN than did HCV- recipients (4/10 HCV+ patients vs. 0/7 HCV- patients; P=0.1). In the HCV+ group, proteinuria was not associated with recurrent HCV hepatitis, DQ matching, posttransplant diabetes, or hypertension. Treatment of HCV-related MPGN with interferon-alpha2b appeared to stabilize proteinuria and renal function but did not reverse renal dysfunction nor cause liver allograft rejection. After transplantation, HCV+ patients had similar renal function over 3 years after transplantation, compared with HCV- patients, but they had an increased risk of proteinuria and occurrence of MPGN that was only partially responsive to interferon.
authors.affiliation: Department of Medicine, University of Washington Medical Center, Seattle 98195, USA.
authors.forename: E A
authors.initials: EA
authors.lastname: Kendrick
authors.forename: J P
authors.initials: JP
authors.lastname: McVicar
authors.forename: K V
authors.initials: KV
authors.lastname: Kowdley
authors.forename: M P
authors.initials: MP
authors.lastname: Bronner
authors.forename: M J
authors.initials: MJ
authors.lastname: Emond
authors.forename: C E
authors.initials: CE
authors.lastname: Alpers
authors.forename: D R
authors.initials: DR
authors.lastname: Gretch
authors.forename: R L
authors.initials: RL
authors.lastname: Carithers
authors.forename: J D
authors.initials: JD
authors.lastname: Perkins
authors.forename: C L
authors.initials: CL
authors.lastname: Davis
mesh_terms: D000328:Adult; D001706:Biopsy; D003404:Creatinine / Q000652:urine; D005260:Female; D005920:Glomerular Mesangium / Q000473:pathology; D015432:Glomerulonephritis, Membranoproliferative / Q000188:drug therapy / Q000652:urine / Q000821:virology*; D006683:HLA-DQ Antigens / Q000276:immunology; D006526:Hepatitis C / Q000139:chemically induced / Q000503:physiopathology* / Q000652:urine; D006801:Humans; D006973:Hypertension / Q000209:etiology; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use; D016031:Liver Transplantation / Q000009:adverse effects; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000652:urine; D011994:Recombinant Proteins; D012189:Retrospective Studies; D012598:Sclerosis
chemical_list: D006683:HLA-DQ Antigens; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D003404:Creatinine