Author + information
- Received July 30, 2014
- Revision received November 30, 2014
- Accepted December 2, 2014
- Published online February 10, 2015.
- Frederik H. Verbrugge, MD∗,†,
- Paul Steels, MD‡,
- Lars Grieten, PhD, MSc∗,‡,
- Petra Nijst, MD∗,†,
- W.H. Wilson Tang, MD§ and
- Wilfried Mullens, MD, PhD∗,‡∗ ()
- ∗Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium
- †Doctoral School for Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium
- ‡Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium
- §Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio
- ↵∗Reprint requests and correspondence:
Dr. Wilfried Mullens, Department of Cardiology, Ziekenhuis Oost-Limburg, Schiepse Bos 6, 3600 Genk, Belgium.
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.
Dr. 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.
- Received July 30, 2014.
- Revision received November 30, 2014.
- Accepted December 2, 2014.
- American College of Cardiology Foundation