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The Kidney in Heart Failure pp 27–38Cite as

Renal Hemodynamic Changes in Heart Failure

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Abstract

Heart failure is manifested by a diminished cardiac output and subsequent reduction in peripheral perfusion affecting all organs and biochemically manifested by changes in kidney function. This diminution in perfusion triggers numerous neurohumoral compensatory mechanisms in an attempt to maintain circulatory volume. These counteractive mechanisms involve activation of baroreceptors in the arterial and venous systems as well as the heart and kidney; they result in sodium and water retention. Over time, this volume expansion culminates in the development of edema. Additionally, both vasodilator and vasoconstrictor mechanisms are activated. These include vasoconstrictor systems such as the sympathetic and renin–angiotensin–aldosterone system (RAAS) and vasoconstrictors such as arginine vasopressin and endothelins. Additionally, natriuretic peptides such as atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and prostaglandins are elevated to counterbalance the vasoconstrictor agents. Elevated adrenergic activity further promotes sodium retention by the kidney and augments RAAS activity. Increased activity of the RAAS results in elevated levels of angiotensin II and subsequently aldosterone. This further bolsters retention of sodium and water. ANP inhibits sodium retention by angiotensin II and vasopressin however, its effect is short-lived and not complete. Similarly, increased aldosterone levels are maintained in heart failure unlike what is observed in healthy individuals. Moreover, aldosterone receptor blockade does not completely reverse the effects of aldosterone. Hyponatremia in heart failure is largely the result of decreased free water clearance secondary to elevated levels of prostaglandins and vasopressin. Use of a selective V2 receptor antagonist markedly improves hyponatremia in heart failure. Many of the resultant compensatory mechanisms that are activated when the heart fails are centralized in the kidney as it receives 25% of all cardiac output each cycle. Taken together, these and other mechanisms help the body compensate from the poor perfusion associated with a failing heart.

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Authors and Affiliations

  1. ASH Comprehensive Hypertension Center, Department of Medicine, University of Chicago Medicine, University of Chicago Medical Center, Chicago, IL, USA

    Ivana Lazich

  2. ASH Comprehensive Hypertension Center, Department of Medicine, University of Chicago Medicine, 5841 S. Maryland Avenue, MC1027, Chicago, IL, 60637, USA

    George L. Bakris

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Correspondence to George L. Bakris .

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  1. ASH Comprehensive Hypertension Center, Department of Medicine, University of Chicago Medical Center, 5841 S. Maryland Avenue, MC1027, Chicago, 60637, Illinois, USA

    George L. Bakris

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Lazich, I., Bakris, G.L. (2012). Renal Hemodynamic Changes in Heart Failure. In: Bakris, G. (eds) The Kidney in Heart Failure. Springer, Boston, MA. https://doi.org/10.1007/978-1-4614-3694-2_3

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  • DOI: https://doi.org/10.1007/978-1-4614-3694-2_3

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