Abstract

RENAL sodium loss is an unexpected complication in a patient with the syndrome. This unusual combination suggested an interesting relation between alkalosis with excess calcium ingestion and renal tubular failure. Burnett and his associates,1 in 1949, described several persons with peptic ulcer, in whom, after the ingestion of large amounts of milk and absorbable alkali over many years, a syndrome characterized by hypercalcemia, absence of hypercalciuria, azotemia, alkalosis, nephrocalcinosis, band keratopathy and metastatic calcification developed. Such cases are difficult to differentiate from hyperparathyroidism with peptic ulcer, complicated by nephrocalcinosis and renal failure.2 The milk-alkali syndrome is distinguished from other . . .

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