Low Urinary Calcium Excretion in Bartter's Syndrome

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Abstract
To the Editor: According to a current hypothesis, potassium wasting in Bartter's syndrome is caused primarily by a defect in the active reabsorption of chloride in the ascending segment of the loop of Henle, with ensuing increased distal tubular flow.1 Other characteristics of the syndrome — i.e., increased production of renal prostaglandins, activation of the renin–angiotensin system, and insensitivity to the pressor effect of angiotensin II — are thought to be secondary to the tubular defect.2 Indeed, a convincing imitation of Bartter's syndrome can be induced by the administration of furosemide, which inhibits chloride reabsorption in the last part of . . .

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