The milk-alkali syndrome. A reversible form of acute renal failure
K. Abreo, A. Adlakha, S. Kilpatrick, R. Flanagan, R. Webb and S. Shakamuri
Department of Medicine, Louisiana State University Medical Center, Shreveport.
The 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 primary hyperparathyroidism.
