New Treatment Options for Bartter's Syndrome

Abstract

To the Editor: Bartter's syndrome is a major cause of congenital salt wasting. As a consequence of abnormal salt reabsorption in the thick ascending limb of Henle's loop due to mutations in the luminal sodium–potassium-2–chloride cotransporter (antenatal Bartter's syndrome type I), the luminal potassium channel (antenatal Bartter's syndrome type II), or the basolateral chloride channel (classic Bartter's syndrome type III), the activity of the renin–angiotensin–aldosterone system increases.1 Prostaglandins increase as a consequence of volume contraction, and this increase may itself stimulate renin secretion.2 Unfortunately, prostaglandins block salt reabsorption by mechanisms that are not yet fully understood.1 The clinical problems in . . .