title: Impact of pretransplantation GB virus C infection on the outcome of renal transplantation.
abstract: Among renal transplant recipients with posttransplantation liver disease, the etiology remains unknown in 10 to 16% of patients. The discovery of yet another parenterally transmitted hepatitis virus, GB virus C (GBV-C), has opened avenues to study the prevalence and risk factors for GBV-C infection among patients undergoing renal transplantation and its impact on posttransplantation clinical outcomes. A cohort of 103 randomly selected recipients of kidneys were examined from anti-hepatitis C virus (HCV)-negative donors between 1986 and 1990. Pretransplantation sera were available in 99 of 103 (96%) recipients and were tested for anti-HCV, using a second-generation ELISA, and for GBV-C RNA by reverse transcription PCR. Pretransplantation GBV-C RNA was present in 18 of 99 (18%, 95% confidence interval [CI], 17.2 to 18.8%) recipients. GBV-C RNA was present in 5 of 22 (23%) anti-HCV-positive recipients compared with 13 of 77 (17%) anti-HCV-negative recipients (P = 0.53). The median number of pretransplantation blood transfusion among recipients with GBV-C RNA before transplantation was significantly higher than among recipients without GBV-C RNA (10 versus 7, P = 0.05). Posttransplantation liver disease and non-A, non-B hepatitis (NANBH) was observed in 35 and 18%, respectively, of GBV-C RNA-positive recipients compared with 28 and 10%, respectively, of GBV-C RNA-negative recipients. Using Cox regression analysis, the relative risk (RR) of posttransplantation liver disease among recipients with GBV-C RNA before transplantation was 1.37 (95% CI, 0.55 to 3.41), and posttransplantation NANBH was 2.09 (95% CI, 0.64 to 6.79). The RR of graft loss and death were not increased (0.88 and 0.92, respectively). When adjusted for pretransplantation anti-HCV, the RR of posttransplantation liver disease, NANBH, graft loss, and death did not change appreciably. In summary, although a higher risk of posttransplantation liver disease was observed among recipients with pretransplantation GBV-C infection, the analyses presented here do not allow for a precise estimate of this risk.
authors.affiliation: Division of Nephrology, New England Medical Center, Boston, Massachusetts 02111, USA.
authors.forename: B V
authors.initials: BV
authors.lastname: Murthy
authors.forename: A S
authors.initials: AS
authors.lastname: Muerhoff
authors.forename: S M
authors.initials: SM
authors.lastname: Desai
authors.forename: J
authors.initials: J
authors.lastname: Yamaguchi
authors.forename: I K
authors.initials: IK
authors.lastname: Mushahwar
authors.forename: C H
authors.initials: CH
authors.lastname: Schmid
authors.forename: A S
authors.initials: AS
authors.lastname: Levey
authors.forename: B J
authors.initials: BJ
authors.lastname: Pereira
mesh_terms: D000328:Adult; D001483:Base Sequence; D015331:Cohort Studies; D017931:DNA Primers / Q000235:genetics; D005260:Female; D018067:Flaviviridae / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity; D006085:Graft Survival; D006525:Hepatitis, Viral, Human / Q000209:etiology*; D006801:Humans; D016030:Kidney Transplantation / Q000009:adverse effects*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011379:Prognosis; D012367:RNA, Viral / Q000235:genetics / Q000302:isolation & purification; D012307:Risk Factors
chemical_list: D017931:DNA Primers; D012367:RNA, Viral