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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/24291

Title: Renal sodiumavidity in heart failure: from pathophysiology to treatment strategies
Authors: Mullens, Wilfried
Verbrugge, Frederik Hendrik
Nijst, Petra
Tang, Wai Hong Wilson
Issue Date: 2017
Citation: EUROPEAN HEART JOURNAL, 38(24), p. 1872-1882B
Abstract: 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.
Notes: [Mullens, Wilfried; Verbrugge, Frederik Hendrik; Nijst, Petra] Ziekenhuis Oost Limburg, Dept Cardiol, Schiepse Bos 6, B-3600 Genk, Belgium. [Mullens, Wilfried] Hasselt Univ, Biomed Res Inst, Dept Med & Life Sci, B-3590 Diepenbeek, Belgium. [Nijst, Petra] Hasselt Univ, Doctoral Sch Med & Life Sci, Dept Med & Life Sci, B-3590 Diepenbeek, Belgium. [Tang, Wai Hong Wilson] Cleveland Clin, Heart & Vasc Inst, Dept Cardiovasc Med, 9500 Euclid Ave, Cleveland, OH 44195 USA.
URI: http://hdl.handle.net/1942/24291
DOI: 10.1093/eurheartj/ehx035
ISI #: 000403828700009
ISSN: 0195-668X
Category: A1
Type: Journal Contribution
Appears in Collections: Research publications

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