The milk-alkali syndrome was first identified in 1923, and continues to occur in patients ingesting large amounts of calcium and absorbable alkali, particularly as calcium carbonate. Hypercalcemia, alkalosis, and renal impairment remain hallmarks of the syndrome, which may occur in acute, subacute, and chronic forms. Although the pathophysiology of the milk-alkali syndrome has not been completely studied, it appears to involve complex interactions between ingested calcium and alkali resulting in an impairment in renal calcium and bicarbonate excretion. The diagnosis of the milk-alkali syndrome is based on a history of calcium and alkali ingestion, the presence of characteristic clinical and laboratory features, and the exclusion of other causes of hypercalcemia. Conservative treatment, including discontinuing calcium and alkali ingestion and supportive measures, is usually effective.