Renal hemodynamics in heart failure: implications for treatment

The purpose of this review is to describe the hemodynamic alterations in the kidney which occur in heart failure and to understand the cardiovascular and renal mechanisms responsible for these alterations. Implications for the clinical management of heart failure will be delineated on the basis of the pathophysiologic cardiorenal interactions.

Recent studies have shown that patients with heart failure exhibit abnormal cardiorenal hemodynamics on the basis of numerous pathophysiologic disturbances involving both the cardiovascular and renal systems. Macrovascular stiffening leads to microvascular damage with impairment of renal autoregulation. Diffuse neurohormonal activation occurs of multiple systems, particularly the renin-angiotensin-aldosterone system, sympathetic nervous system, arginine vasopressin system, endothelin system, and natriuretic peptide system, leading to an overall vasoconstrictive state promoting sodium and water retention and further impairment of cardiac function. Pharmacologic therapy directed at specific biochemical targets within these neurohormonal pathways has shown marked benefits in improving both the symptoms of heart failure and clinical outcomes.

Heart failure is characterized by abnormal cardiovascular hemodynamics, sodium and fluid retention, and diffuse neurohormonal activation, all of which affect the net renal hemodynamic state. An understanding of the pathophysiologic mechanisms is necessary to optimally manage patients with heart failure and help restore cardiorenal homeostasis.