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Heart Fail Rev. 2012 Mar;17(2):161-75. doi: 10.1007/s10741-011-9246-2.

Systemic arterial and venous determinants of renal hemodynamics in congestive heart failure.

Author information

1
Department of Medicine/Division of Nephrology and Immunology, University of Alberta Hospital, 11-132 CSB Clinical Sciences Building, Edmonton, AB T6G 2G3, Canada. branko.braam@ualberta.ca

Abstract

Heart and kidney interactions are fascinating, in the sense that failure of the one organ strongly affects the function of the other. In this review paper, we analyze how principal driving forces for glomerular filtration and renal blood flow are changed in heart failure. Moreover, renal autoregulation and modulation of neurohumoral factors, which can both have repercussions on renal function, are analyzed. Two paradigms seem to apply. One is that the renin-angiotensin system (RAS), the sympathetic nervous system (SNS), and extracellular volume control are the three main determinants of renal function in heart failure. The other is that the classical paradigm to analyze renal dysfunction that is widely applied in nephrology also applies to the pathophysiology of heart failure: pre-renal, intra-renal, and post-renal alterations together determine glomerular filtration. At variance with the classical paradigm is that the most important post-renal factor in heart failure seems renal venous hypertension that, by increasing renal tubular pressure, decreases GFR. When different pharmacological strategies to inhibit the RAS and SNS and to assist renal volume control are considered, there is a painful lack in knowledge about how widely applied drugs affect primary driving forces for ultrafiltration, renal autoregulation, and neurohumoral control. We call for more clinical physiological studies.

PMID:
21553212
DOI:
10.1007/s10741-011-9246-2
[Indexed for MEDLINE]

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