Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/18662
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dc.contributor.authorVERBRUGGE, Frederik-
dc.contributor.authorSTEELS, Paul-
dc.contributor.authorGRIETEN, Lars-
dc.contributor.authorNIJST, Petra-
dc.contributor.authorTang, W. H. Wilson-
dc.contributor.authorMULLENS, Wilfried-
dc.date.accessioned2015-04-10T10:45:08Z-
dc.date.available2015-04-10T10:45:08Z-
dc.date.issued2015-
dc.identifier.citationJOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 65 (5), p. 480-492-
dc.identifier.issn0735-1097-
dc.identifier.urihttp://hdl.handle.net/1942/18662-
dc.description.abstractHyponatremia frequently poses a therapeutic challenge in acute decompensated heart failure (ADHF). Treating physicians should differentiate between depletional versus dilutional hyponatremia. The former is caused by diuretic agents, which enhance sodium excretion, often with concomitant potassium/magnesium losses. This can be treated with isotonic saline, whereas potassium/magnesium administration may be helpful if plasma concentrations are low. In contrast, as impaired water excretion, rather than sodium deficiency, is the culprit in dilutional hyponatremia, isotonic saline administration may further depress the serum sodium concentration. Because free water excretion is achieved by continuous sodium reabsorption in distal nephron segments with low water permeability, diuretic agents that impair this mechanism (e.g., thiazide-type diuretic agents and mineralocorticoid receptor antagonists) should be avoided, and proximally acting agents (e.g., acetazolamide and loop diuretic agents) are preferred. Vasopressin antagonists, which promote low water permeability in the collecting ducts and, hence, free water excretion, remain under investigation for dilutional hyponatremia in ADHF. (C) 2015 by the American College of Cardiology Foundation.-
dc.description.sponsorshipDr. Verbrugge is supported by a PhD fellowship from the Research Foundation-Flanders. Drs. Verbrugge, Grieten, Nijst, and Mullens are researchers for the Limburg Clinical Research Program UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk, Hasselt University, Ziekenhuis Oost-Limburg, and Jessa Hospital. Drs. Steels and Tang have reported that they have no relationships relevant to the contents of this paper to disclose.-
dc.language.isoen-
dc.publisherELSEVIER SCIENCE INC-
dc.rights© 2015 by the American College of Cardiology Foundation.-
dc.subject.otherarginine vasopressin; distal; diuretics; kidney tubules; physiopathology; sodium-
dc.titleHyponatremia in Acute Decompensated Heart Failure Depletion Versus Dilution-
dc.typeJournal Contribution-
dc.identifier.epage492-
dc.identifier.issue5-
dc.identifier.spage480-
dc.identifier.volume65-
local.format.pages13-
local.bibliographicCitation.jcatA1-
dc.description.notes[Verbrugge, Frederik H.; Grieten, Lars; Nijst, Petra; Mullens, Wilfried] Ziekenhuis Oost Limburg, Dept Cardiol, B-3600 Genk, Belgium. [Verbrugge, Frederik H.; Steels, Paul; Nijst, Petra] Hasselt Univ, Doctoral Sch Med & Life Sci, Diepenbeek, Belgium. [Mullens, Wilfried] Hasselt Univ, Doctoral Sch Med & Life Sci, Fac Med & Life Sci, Biomed Res Inst, Diepenbeek, Belgium. [Tang, W. H. Wilson] Cleveland Clin, Inst Heart & Vasc, Dept Cardiovasc Med, Cleveland, OH USA.-
local.publisher.placeNEW YORK-
local.type.refereedRefereed-
local.type.specifiedReview-
dc.identifier.doi10.1016/j.jacc.2014.12.010-
dc.identifier.isi000348667000014-
item.validationecoom 2016-
item.contributorVERBRUGGE, Frederik-
item.contributorSTEELS, Paul-
item.contributorGRIETEN, Lars-
item.contributorNIJST, Petra-
item.contributorTang, W. H. Wilson-
item.contributorMULLENS, Wilfried-
item.accessRightsRestricted Access-
item.fullcitationVERBRUGGE, Frederik; STEELS, Paul; GRIETEN, Lars; NIJST, Petra; Tang, W. H. Wilson & MULLENS, Wilfried (2015) Hyponatremia in Acute Decompensated Heart Failure Depletion Versus Dilution. In: JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 65 (5), p. 480-492.-
item.fulltextWith Fulltext-
crisitem.journal.issn0735-1097-
crisitem.journal.eissn1558-3597-
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