Bartter's syndrome is a congenital abnormality characterized by metabolic 
alkalosis [corrected], hyperreninemic hyperaldosteronism, and hypokalemia. Most 
patients present early in life with symptoms such as muscle weakness and 
polyuria, which may be attributed to potassium depletion. Despite the 
hyperaldosteronism, the patients tend to be normotensive, which is at least 
partially explained by vascular hyporesponsiveness to pressor hormones. Numerous 
studies have documented increased renal excretion of prostaglandins. Several 
different patterns of aberrant renal ion transport have been observed in 
patients with the syndrome, suggesting that it actually may represent a family 
of related but distinct tubular disorders. Therapeutic approaches to Bartter's 
syndrome include potassium supplementation, prostaglandin synthesis inhibitors 
(nonsteroidal anti-inflammatory agents), aldosterone antagonists, and converting 
enzyme inhibitors. During the first two decades following its initial 
description, Bartter's syndrome was the focus of widespread interest, based on 
the likelihood that its investigation might provide insight into the normal 
functioning of the renin-angiotensin-aldosterone and prostanoid hormone systems. 
During the past decade, however, little additional progress has been made in 
Bartter's syndrome, and its patho-physiology remains poorly understood.