Renal sodium avidity in heart failure: from pathophysiology to treatment strategies

Wilfried Mullens, Frederik Hendrik Verbrugge, Petra Nijst, Wai Hong Wilson Tang

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102 Citations (Scopus)


Increased neurohumoral stimulation resulting in excessive sodium avidity and extracellular volume overload are hallmark features of decompensated heart failure. Especially in case of concomitant renal dysfunction, the kidneys often fail to elicit effective natriuresis. While assessment of renal function is generally performed by measuring serum creatinine-a surrogate for glomerular filtration-, this only represents part of the nephron's function. Alterations in tubular sodium handling are at least equally important in the development of volume overload and congestion. Venous congestion and neurohumoral activation in advanced HF further promote renal sodium and water retention. Interestingly, early on, before clinical signs of heart failure are evident, intrinsic renal derangements already impair natriuresis. This clinical review discusses the importance of heart failure (HF) induced changes in different nephron segments. A better understanding of cardiorenal interactions which ultimately result in sodium avidity in HF might help to treat and prevent congestion in chronic and acute HF.

Original languageEnglish
Pages (from-to)1872-1882
Number of pages11
JournalEuropean Heart Journal
Issue number24
Publication statusPublished - 21 Jun 2017

Bibliographical note

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions, please email:


  • Acute Disease
  • Cardio-Renal Syndrome/drug therapy
  • Diuretics/therapeutic use
  • Glomerular Filtration Rate/physiology
  • Homeostasis/physiology
  • Humans
  • Kidney Glomerulus/physiology
  • Kidney Tubules/physiology
  • Phenotype
  • Renal Circulation/physiology
  • Renal Insufficiency, Chronic/physiopathology
  • Sodium/metabolism
  • Sodium Potassium Chloride Symporter Inhibitors/therapeutic use


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