SAMI A. SANJAD, M.D.; BRUCE S. KEENAN, M.D.; L. LEIGHTON HILL, M.D.
Grant support: in part by the Beta Sigma Phi Metabolic Research Fund 520-G01149, Baylor College of Medicine; and grant USPH5M01RR0188 from the Children's Clinical Research Center, Texas Children's Hospital.
Presented in part November 1981 at the American Society of Nephrology Meeting, Washington, D.C.
▸Requests for reprints should be addressed to Sami A. Sanjad, M.D.; Department of Pediatrics, Baylor College of Medicine, 1200 Morslund Avenue; Houston, TX 77030.
SANJAD SA, KEENAN BS, HILL LL. Renal Hypoprostaglandism, Hypertension, and Type IV Renal Tubular Acidosis Reversed by Furosemide. Ann Intern Med. 1983;99:624-627. doi: 10.7326/0003-4819-99-5-624
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Published: Ann Intern Med. 1983;99(5):624-627.
A 13-year-old white girl with severe hypertension and type IV renal tubular acidosis had decreased renal chloride clearance and exaggerated sodium chloride reabsorption by the ascending limb of Henle during hypotonic saline diuresis. Urinary prostaglandin E2 excretion was markedly diminished and often undetectable (0 to 37 ng/24 h). Treatment with oral furosemide completely reversed the hypertension and hyperkalemic acidosis, and effected a 20-fold rise in urinary prostaglandin E2. Sodium chloride reabsorption by the thick ascending limb of Henle decreased from 93.5% to 79.3%. Renal hypoprostaglandism may have a pathogenic role in this syndrome by enhancing chloride reabsorption in the ascending limb of Henle leading to extracellular fluid volume expansion, hypertension, and suppression of the renin-angiotensin-aldosterone axis. The therapeutic effects of furosemide may be partially mediated by enhancing the biosynthesis of renal prostaglandins or inhibiting their breakdown.
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Cardiology, Endocrine and Metabolism, Nephrology, Hypertension, Adrenal Disorders.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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