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  • Title: Renal allograft survival in patients with oxalosis.
    Author: Cibrik DM, Kaplan B, Arndorfer JA, Meier-Kriesche HU.
    Journal: Transplantation; 2002 Sep 15; 74(5):707-10. PubMed ID: 12352890.
    Abstract:
    BACKGROUND: Primary hyperoxaluria is a rare autosomal recessive metabolic disease that often progresses to end-stage renal disease (ESRD). Liver transplantation is curative for patients with the alanine: glyoxylate aminotransferase deficiency. For oxalosis patients with minor enzyme deficiencies, renal transplantation may be the therapy of choice although concern exists about recurrence of oxalosis in the transplanted kidney. To date, previous data has been conflicting with most reports indicating poor renal allograft survival for oxalosis patients who receive a renal transplant alone. To determine whether graft survival in renal transplant recipients with oxalosis is similar to other transplant recipients with other forms of ESRD, we analyzed the United States Renal Data System (USRDS) registry comparing death-censored graft survival for transplant recipients with oxalosis to a reference group with ESRD secondary to glomerulonephritis (GN). METHODS: Using the USRDS and the U.S. Scientific Renal Transplant Registry data, we found 190 adult renal transplant recipients from 1988 to 1998 who had oxalosis as their primary diagnosis for their ESRD. Among the patients with oxalosis, 56 patients had a liver transplant followed by a kidney transplant (LKTx) and 134 patients had a kidney transplant alone (KTA). A Cox proportional hazard model was used to estimate patient survival and death-censored graft survival for patients with oxalosis who received a LKTx or a KTA. Unadjusted death-censored graft survival for oxalosis patients with a cadaveric or living-donor KTA or with a LKTx was obtained from Kaplan-Meier analysis. Recipients of solitary kidney transplants with GN served as the reference group. RESULTS: Oxalosis patients receiving a KTA had a significantly worse adjusted death-censored graft survival (47.9%) compared with patients with GN (61%) at 8 years posttransplantation (P <0.001). In contrast, oxalosis patients who received a LKTx had a significantly higher death-censored graft survival (76%) compared with oxalosis patients who received a KTA (47.9%, P<0.001) and had a trend toward better death-censored graft survival compared with patients with GN (P =0.05). In addition, oxalosis patients who received a living-donor KTA had significantly worse death-censored graft survival compared with oxalosis patients who received a LKTx (22% vs. 64%, P<0.01). Patient survival for oxalosis recipients with a KTA or a LKTx was not significantly different. CONCLUSIONS: Patients with oxalosis who receive a LKTx have superior death-censored graft survival compared with oxalosis patients who receive a cadaveric or living-donor KTA and trended toward better graft survival compared with GN patients.
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