ALLEN C. ALFREY, M.D.; DAVID S. TERMAN, M.D.; LAWRENCE BRETTSCHNEIDER, M.D.; KENNETH M. SIMPSON, M.D.; DAVID A. OGDEN, M.D., F.A.C.P.
The clinical and biochemical features of three patients who developed magnesium intoxication after renal homotransplantation are described. All patients were receiving magnesium-containing antacids at a time when renal function was reduced. When renal function was adequate, magnesium supplementation in the form of antacids resulted in an eightfold increase in urinary magnesium and only a modest rise in serum levels. However, during transplant rejection urinary magnesium rapidly falls, and hypermagnesemia may develop. Hemodialysis is the most effective method of treating this complication in the transplant recipient. Magnesium intoxication represents an additional hazard of high-dose antacid therapy in the postransplant period. The serum magnesium concentration should be routinely monitored in transplant recipients with reduced renal function receiving magnesium-containing antacid. At times of severely compromised renal function these antacids should be avoided.
ALLEN C. ALFREY, DAVID S. TERMAN, LAWRENCE BRETTSCHNEIDER, KENNETH M. SIMPSON, DAVID A. OGDEN. Hypermagnesemia After Renal Homotransplantation. Ann Intern Med. 1970;73:367–371. doi: 10.7326/0003-4819-73-3-367
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Published: Ann Intern Med. 1970;73(3):367-371.
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