A Reversible Form of Acute Renal Failure

milk-alkali syndrome became rare with the advent of modern ulcer therapy with nonabsorbable antacids, histamine2 blockers, and sucralfate. An increased frequency of this syndrome seems likely with the growing popularity of the use of calcium carbonate as an antacid or as calcium supplementation to prevent osteoporosis. We treated five patients who had six episodes of the milk-alkali syndrome; four of these cases were diagnosed between 1990 and 1992. All patients were ingesting massive quantities of calcium and absorbable alkali and were unaware of the toxic effects of these compounds. All patients presented with the triad of hypercalcemia, metabolic alkalosis, and renal failure. All metabolic abnormalities were corrected, and renal function improved with appropriate supportive measures and cessation of calcium and alkali ingestion. In two patients, the renal failure was so severe that dialysis was necessary. In four patients, either the serum amino-terminal parathyroid hormone or 1,25-dihydroxycholecalciferol levels were appropriately decreased in response to hypercalcemia. The serum carboxy-terminal parathyroid hormone levels were increased because of renal failure. Since both physicians and patients are often unaware of the calcium and alkali content of many nonprescription medicines, the diagnosis of the milk-alkali syndrome, a reversible cause of renal failure, can be missed if a detailed history of such intake is not elicited. Measurement of the serum amino-terminal parathyroid hormone and 1,25-dihydroxycholecalciferol levels may help differentiate milk-alkali syndrome from