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Sucralfate, Intestinal Aluminum Absorption, and Aluminum Toxicity in a Patient on Dialysis

John A. Robertson, MD; Isidro B. Salusky, MD; William G. Goodman, MD; Keith C. Norris, MD; and Jack W. Coburn, MD
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Grant Support: Supported in part by research funds from the Veterans Administration; U.S.P.H.S. grants M01RR00865, DK 35423, and AR35470; and the Peter Boxenbaum Research Fund.

Requests for Reprints: Jack W. Coburn, MD, Nephrology Section 691/ W11L, West Los Angeles Veterans Administration Medical Center, Wadsworth Division, Wilshire and Sawtelle Boulevards, Los Angeles, CA 90073.

Current Author Addresses: Dr. Robertson: 4000 Fourteenth Street, Suite 206, Riverside, CA 92501.

Dr. Salusky: UCLA Center for Health Sciences, A2-373 MDCC, Westwood, Los Angeles, CA 90024.

Dr. Goodman: Nephrology Section 111R, Veterans Administration Medical Center, Sepulveda, 16111 Plummer Street, Sepulveda, CA 91343.

Drs. Norris and Coburn: Nephrology Section W111L, Veterans Administration Medical Center, West Los Angeles, Wilshire and Sawtelle Boulevards, Los Angeles, CA 90073.

Ann Intern Med. 1989;111(2):179-181. doi:10.7326/0003-4819-111-2-179
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This excerpt has been provided in the absence of an abstract.

Aluminum absorption from aluminum-containing phosphate-binding antacids is a major source of aluminum loading in patients on dialysis (1). The aluminum is retained when renal function is impaired, and it has been implicated in the pathogenesis of osteomalacia and encephalopathy in these patients (2). Sucralfate, the basic aluminum salt of sucrose sulfate, contains 21% aluminum by weight (3); it is widely used to treat peptic ulcer disease and gastritis (4). Sucralfate does not alter plasma aluminum levels in normal subjects (5). Aluminum can dissociate, however, from sucralfate at a low pH (6) and become bioavailable. Our case report and study data


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