Bartter's syndrome. Study of a 52 year old man with evidence for a defect in proximal tubular sodium reabsorption and comments on therapy.

A patient with Bartter's syndrome in whom the disease was recognized at 52 years of age is described. Studies of his renal function suggest that the basic pathophysiologic defect was an abnormality in proximal tubular sodium reabsorption which led to extracellular fluid volume depletion and consequent stimulation of the renin-angiotensin-aldosterone axis. After comparing the physiologic studies in this patient with those in other reported cases, we postulate that Bartter's syndrome may represent the end result of different pathophysiologic processes which share in common juxtaglomerular hyperplasia, increased renin release and secondary hyperaldosteronism. Therapy with B-adrenergic blocking agents produced adverse effects, but the patient responded well to more conventional measures.