Renal sodium avidity in heart failure: from pathophysiology to treatment strategies.
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.
Department of Cardiology, Ziekenhuis Oost-Limburg, Schiepse Bos 6, 3600 Genk, Belgium.|Department of Medicine and Life Sciences, Biomedical Research Institute, Hasselt University, Agoralaan Gebouw D, 3590 Diepenbeek, Belgium.
Wilfried
W
Mullens
Department of Cardiology, Ziekenhuis Oost-Limburg, Schiepse Bos 6, 3600 Genk, Belgium.
Frederik Hendrik
FH
Verbrugge
Department of Cardiology, Ziekenhuis Oost-Limburg, Schiepse Bos 6, 3600 Genk, Belgium.|Department of Medicine and Life Sciences, Doctoral School for Medicine and Life Sciences, Hasselt University, Agoralaan Gebouw D, 3590 Diepenbeek, Belgium.
Petra
P
Nijst
Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, 44195 Ohio, USA.
Wai Hong Wilson
WHW
Tang
D000208:Acute Disease; D059347:Cardio-Renal Syndrome / Q000188:drug therapy / Q000503:physiopathology*; D004232:Diuretics / Q000627:therapeutic use; D005919:Glomerular Filtration Rate / Q000502:physiology; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007678:Kidney Glomerulus / Q000502:physiology; D007684:Kidney Tubules / Q000502:physiology; D010641:Phenotype; D012079:Renal Circulation / Q000502:physiology; D051436:Renal Insufficiency, Chronic / Q000503:physiopathology; D012964:Sodium / Q000378:metabolism*; D049994:Sodium Potassium Chloride Symporter Inhibitors / Q000627:therapeutic use
D004232:Diuretics; D049994:Sodium Potassium Chloride Symporter Inhibitors; D012964:Sodium
Diuretic; Glomerulus; Heart failure; Kidney; Natriuresis; Sodium