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Bartter's Syndrome: Urinary Prostaglandin E-like Material and Kallikrein; Indomethacin Effects

PERRY V. HALUSHKA, M.D., Ph.D.; HULDA WOHLTMANN, M.D.; PHILIP J. PRIVITERA, Ph.D.; GILBERT HURWITZ, M.D.; and HARRY S. MARGOLIUS, M.D., Ph.D.
[+] Article and Author Information

Grant support: by Grants GM20387 and HL17705. Dr. Halushka is a recipient of a Pharmaceutical Manufacturers Association Foundation Faculty Development Award in Clinical Pharmacology. Dr. Margolius is a Burroughs Wellcome Scholar in Clinical Pharmacology.

Presented in part at the Fifth International Congress of Endocrinology, Hamburg, Germany, July 1976; and the American Society for Pharmacology and Experimental Therapeutics Meeting, New Orleans, Louisiana, 17, August 1976.

▸Requests for reprints should be addressed to Perry V. Haluska, M.D., Ph.D.; Department of Basic and Clinical Pharmacology; Medical University of South Carolina; 80 Barre Street; Charleston, SC 29401.


Charleston, South Carolina


Ann Intern Med. 1977;87(3):281-286. doi:10.7326/0003-4819-87-3-281
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The urinary excretions of prostaglandin E-like material (iPGE) and kallikrein were measured in two children with Bartter's syndrome. Urinary iPGE excretion was three and 10 times greater than normal, and urinary kallikrein was five and 10 times greater than normal in the two subjects. Furthermore, excretions of iPGE and kallikrein were highly correlated (P < 0.005) with each other before and during treatment with indomethacin, a prostaglandin synthetase inhibitor. Indomethacin significantly (P < 0.001) reduced urinary iPGE, urinary kallikrein, and plasma renin activity, while increasing the sensitivity to intravenous angiotensin II and the serum potassium to normal. The results confirm that renal prostaglandins may be involved in the pathogenesis of Bartter's syndrome and suggest that renal prostaglandins and the kallikrein-kinin system are linked.

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