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Eduardo H. Garin, MD; Robert S. Fennell III; Abdollah Iravani, MD; George A. Richard, MD

Am J Dis Child. 1980;134(3):258-261.

Abstract
• Two patients with Bartter's syndrome were treated with indomethacin (2 mg/kg/day). The administration of the drug resulted in weight gain; a decrease in the rate of urinary excretion of sodium and inorganic phosphate suggesting an increase in proximal tubular reabsorption; an increase in serum potassium concentration, with a transient decrease in the rate of urinary potassium excretion in one patient; and a decrease in plasma renin activity and in the rate of urinary aldosterone excretion. Since indomethacin has been shown to inhibit prostaglandin synthetase, these observations support the hypothesis that prostaglandin excess is a basic pathogenic mechanism in Bartter's syndrome.

(Am J Dis Child 134:258-261, 1980)

Author Affiliations
From the Division of Nephrology, Department of Pediatrics, University of Florida College of Medicine, Gainesville.

Footnotes
Reprint requests to Division of Nephrology, Department of Pediatrics, University of Florida College of Medicine, Box J-296, Gainesville, FL 32610 (Dr Garin).

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