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Acute Oxalate Nephropathy: A New Etiology for Acute Renal Failure Following Nonrenal Solid Organ Transplantation
Article first published online: 1 AUG 2006
DOI: 10.1111/j.1600-6143.2006.01485.x
Additional Information
How to Cite
Lefaucheur, C., Hill, G. S., Amrein, C., Haymann, J.-P., Jacquot, C., Glotz, D. and Nochy, D. (2006), Acute Oxalate Nephropathy: A New Etiology for Acute Renal Failure Following Nonrenal Solid Organ Transplantation. American Journal of Transplantation, 6: 2516–2521. doi: 10.1111/j.1600-6143.2006.01485.x
Publication History
- Issue published online: 1 AUG 2006
- Article first published online: 1 AUG 2006
- Received 3 April 2006, revised 25 May 2006 and accepted for publication 12 June 2006
- Abstract
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Keywords:
- Acute renal failure;
- oxalate nephropathy
In three non-renal transplants, irreversible acute renal insufficiency developed in relationship to enteric hyperoxaluria associated with prolonged post-operative antibiotic use.
Acute renal insufficiency (ARI) is a frequent complication of nonrenal solid organ transplantation and may be responsible for an unfavorable outcome, particularly if dialysis is required. The etiology of post-transplantation ARI is poorly understood, with only isolated clinical cases being reported, most imputed to drug toxicity. We report here, the first three observations of irreversible ARI associated with acute oxalate nephropathy (AON) in the course of nonrenal organ transplants: a lung transplant and a lung-liver transplant in two patients with mucoviscidosis, and a cardiac transplant. The diagnosis of AON was made histologically. In all three cases, the ARI supervened after prolonged consumption of antibiotics capable of interfering with the colonic flora, and leading to enteric hyperoxaluria.
The recognition of AON as a cause of post-transplantation, ARI underlines hyperoxaluria and digestive hyperabsorption of oxalate as specific risk factors for AON and should permit better posttransplant care of these patients.