title: Potential for bilateral nephrectomy to reduce oxalate release after combined liver and kidney transplantation for primary hyperoxaluria type 1.
abstract: Primary hyperoxaluria type 1 (PH-1) is frequently associated with end stage renal failure due to urinary calculi, obstructive uropathy and interstitial deposits of calcium oxalate. The currently accepted treatment for PH-1 is liver transplantation to replace the deficient enzyme peroxisomal alanine glycoxylate aminotransferase (AGT) and a simultaneous renal transplant to restore renal function. The transplanted kidney may become significantly impaired or fail when systemic calcium oxalate is eliminated by renal excretion. The native kidneys are a major source of this oxalate. This study was undertaken to determine whether there is a difference in oxalate clearance following combined liver-kidney transplant in patients with PH-1 by comparing the effect of native kidney nephrectomy at the time of transplantation against leaving the native kidneys in situ. Regression analysis was used to compare daily urinary oxalate excretion corrected for body surface area. There was a significant reduction in urinary oxalate excretion (P < 0.05) in the patient who had undergone bilateral nephrectomy compared to the patient whose native kidneys remained in situ for the first 100 d following combined liver and kidney transplantation. No difference was observed in the serum oxalate levels between patients over the same period or in the renal function assessed by creatinine clearance corrected for body surface area. Total body oxalate load was not determined in this study. A larger study should be undertaken to examine the benefits of nephrectomy in reducing oxalate deposition in recently inserted allografts for patients with PH-1.
authors.affiliation: Renal Transplantation Unit, Princess Alexandra Hospital, Woolloongabba, Australia.
authors.forename: Y
authors.initials: Y
authors.lastname: Mizusawa
authors.forename: A P
authors.initials: AP
authors.lastname: Parnham
authors.forename: M C
authors.initials: MC
authors.lastname: Falk
authors.forename: J R
authors.initials: JR
authors.lastname: Burke
authors.forename: D
authors.initials: D
authors.lastname: Nicol
authors.forename: J
authors.initials: J
authors.lastname: Yamanaka
authors.forename: S V
authors.initials: SV
authors.lastname: Lynch
authors.forename: R W
authors.initials: RW
authors.lastname: Strong
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000172:deficiency; D001830:Body Surface Area; D002129:Calcium Oxalate / Q000097:blood / Q000378:metabolism* / Q000652:urine; D002675:Child, Preschool; D003404:Creatinine / Q000097:blood / Q000652:urine; D017583:Hemodiafiltration; D006801:Humans; D006960:Hyperoxaluria, Primary / Q000150:complications / Q000201:enzymology / Q000503:physiopathology / Q000601:surgery*; D007668:Kidney / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000209:etiology; D016030:Kidney Transplantation / Q000502:physiology; D016031:Liver Transplantation; D008297:Male; D009392:Nephrectomy / Q000379:methods*; D009395:Nephritis, Interstitial / Q000209:etiology; D009397:Nephrocalcinosis / Q000209:etiology; D012044:Regression Analysis; D014184:Transplantation, Homologous; D014545:Urinary Calculi / Q000209:etiology
chemical_list: D002129:Calcium Oxalate; D003404:Creatinine; D000410:Alanine Transaminase