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Acute Oxalate Nephropathy After Massive Ascorbic Acid Administration
John M. Lawton, MD;
Lars T. Conway, MD;
John T. Crosson, MD;
Charles L. Smith, MD;
Paul A. Abraham, MD
Arch Intern Med. 1985;145(5):950-951.
Abstract
• A single 45-g dose of intravenous ascorbic acid, a metabolic precursor of oxalate, was administered to a patient as adjuvant therapy for primary amyloidosis and the nephrotic syndrome. Acute oliguric renal failure occurred. Postmortem histopathologic examination of renal tissue revealed extensive intratubular deposition of crystalline material, which was confirmed as calcium oxalate by a microincineration technique. There were no extrarenal deposits of calcium oxalate. Plasma oxalate and ascorbic acid concentrations were increased. We conclude that therapy with high-dose ascorbic acid is a potential cause of oxalate nephropathy.
(Arch Intern Med 1985;145:950-951)
Author Affiliations
From the Regional Kidney Disease Program (Drs Lawton, Smith, and Abraham) and the Department of Pathology (Drs Conway and Crosson), Hennepin County Medical Center, Minneapolis.
Footnotes
Accepted for publication Sept 10, 1984.
Reprint requests to Regional Kidney Disease Program, Hennepin County Medical Center, 701 Park Ave, Minneapolis, MN 55415 (Dr Abraham).
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