Bartter's Syndrome

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Abstract
Two brothers had evidence of Bartter's syndrome. Rapid intravenous infusions of saline reverted angiotensin insensitivity and elevated plasma renin activity to normal levels, suggesting that secondary stimulation of the renin-angiotensin-aldosterone system by a decreased extracellular volume (ECFV) may be a major defect in these patients. The data indicate that chronic ECFV depletion exists as a consequence of impaired distal sodium reabsorption. However, inexorable sodium loss does not occur, presumably due to enhanced proximal sodium reabsorption. The patients also exhibited renal wasting of potassium, in part independent of the effects of aldosterone. Bartter's syndrome appears to be the result of renal tubular defects in the handling of sodium and potassium. Evidence presented suggests this defect lies beyond the proximal part of the nephron.