title: Hyponatremia in acute decompensated heart failure: depletion versus dilution.
abstract: Hyponatremia 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.
authors: Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium; Doctoral School for Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium.
authors: Frederik H
authors: FH
authors: Verbrugge
authors: Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium.
authors: Paul
authors: P
authors: Steels
authors: Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium; Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium.
authors: Lars
authors: L
authors: Grieten
authors: Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium; Doctoral School for Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium.
authors: Petra
authors: P
authors: Nijst
authors: Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
authors: W H Wilson
authors: WH
authors: Tang
authors: Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium; Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium. Electronic address: wilfried.mullens@zol.be.
authors: Wilfried
authors: W
authors: Mullens
mesh_terms: D000208:Acute Disease; D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood; D004232:Diuretics / Q000009:adverse effects; D006333:Heart Failure / Q000097:blood / Q000150:complications* / Q000188:drug therapy*; D006801:Humans; D007010:Hyponatremia / Q000097:blood / Q000139:chemically induced* / Q000150:complications*; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D049994:Sodium Potassium Chloride Symporter Inhibitors / Q000009:adverse effects
chemical_list: D004232:Diuretics; D000451:Mineralocorticoid Receptor Antagonists; D049994:Sodium Potassium Chloride Symporter Inhibitors; D001127:Arginine Vasopressin
keywords: arginine vasopressin; distal; diuretics; kidney tubules; physiopathology; sodium