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Previous Volume 343:661-662 August 31, 2000 Number 9 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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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 . . . [Full Text of this Article]

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