Letters and Corrections1 May 1989Thiazide-Induced Hyponatremia and Vasopressin ReleaseMoshe Sonnenblick, MD, Nurith Algur, MSc, Arnold Rosin, MDMoshe Sonnenblick, MDSearch for more papers by this author, Nurith Algur, MScSearch for more papers by this author, Arnold Rosin, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-110-9-571_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor: We read with interest the report of Friedman and colleagues (1) on thiazide-induced hyponatremia. Although they ascribe the pathogenesis of thiazide-induced hyponatremia to excess drinking, they did not monitor water intake. It is also surprising that the free water clearance was not more significantly reduced in the "patients," an expected accompaniment when serum sodium is diluted. The authors also cited evidence that the hyponatremia was not due to excess sodium excretion and concluded that excess antidiuretic hormone (ADH, vasopressin) activity did not play a part in the pathogenesis.We have previously reported (2) a number of elderly...References1. FriedmanShadelHalkinFarfel EMHF. Thiazide induced hyponatremia: reproducibility by single-dose rechallenge and an analysis of pathogenesis. Ann Intern Med. 1989;110:24-9. LinkGoogle Scholar2. SonnenblickRosin MA. Significance of the measurement of uric acid fractional clearance in diuretic induced hyponatremia. Postgrad Med J. 1986;62:449-52. CrossrefMedlineGoogle Scholar3. SonnenblickRosin MA. Increased uric acid clearance in the syndrome of inappropriate secretion of antidiuretic hormone. Isr J Med Sci. 1988;24:20-3. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Shaare Zedek Medical Center Jerusalem Israel PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByThiazide-Associated Hyponatremia: Clinical Manifestations and PathophysiologyFluid, Electrolyte, and Acid–Base DisordersA systematic review and meta-analysis of thiazide-induced hyponatraemia: time to reconsider electrolyte monitoring regimens after thiazide initiation?Severe Hyponatremia Associated with Thiazide Diuretic UseFluid, Electrolyte, and Acid–Base DisordersHyponatremia Induced by DrugsHyponatremiaHyponatremia and the Use of Vasopressin Receptor Antagonists In Critically Ill PatientsDiuretics in clinical practice. Part II: electrolyte and acid-base disorders complicating diuretic therapyThiazide-Induced HyponatremiaCopeptin in the Differential Diagnosis of HyponatremiaBlood pressure drug therapy and electrolyte disturbancesThe Silent Epidemic of Thiazide-Induced HyponatremiaHyponatremiaThiazides: do they kill?Risk factors for thiazide-induced hyponatraemiaFluid, Electrolyte, and Acid-Base DisordersDiuretic induced hyponatraemia in elderly hypertensive womenFluid, Electrolyte, and Acid-Base DisordersDefective post-diuretic antinatriuresis in the aging kidney: a possible explanation for thiazide-induced hyponatremia in the elderlyFluid, Electrolyte, and Acid-Base DisordersDiuretic-induced Severe HyponatremiaPost-marketing surveillance of quinolones 1988–1990Diuretic drugs 1 May 1989Volume 110, Issue 9Page: 751-751KeywordsAntidiuretic hormoneElderlyExcretionHyponatremiaPathogenesisSodiumVasopressin Issue Published: 1 May 1989 PDF DownloadLoading ...
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