MALCOLM COX, M.D.; JOSEPH GUZZO, M.D.; GAIL MORRISON, M.D.; IRWIN SINGER, M.D.
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To the editor: Demeclocycline is known to cause nephrogenic diabetes insipidus in humans and to inhibit ADH-induced osmotic water flow in the toad urinary bladder (1). The drug has been used successfully in the treatment of the syndrome of inappropriate antidiuretic hormone secretion (2-4), allowing patients free access to water. Recently De Troyer and colleagues (5) have reported that demeclocycline causes both a water and a sodium diuresis in patients with cirrhosis. However, there was no change in plasma sodium concentration despite the production of a hypotonic urine (mean urine osmolality, 183 mosmol/kg). Even assuming that the patients excreted no urea (that is, attributing all the urine osmolality [Uosm] to electrolytes) and had zero insensible water loss, it is difficult to understand why the plasma
COX M, GUZZO J, MORRISON G, et al. Demeclocycline and Therapy of Hyponatremia. Ann Intern Med. 1977;86:113–114. doi: 10.7326/0003-4819-86-1-113
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Published: Ann Intern Med. 1977;86(1):113-114.
Endocrine and Metabolism, Fluid and Electrolyte Disorders, Nephrology.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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