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Cardiorenal Connections

Salt and Water Retention

Renal retention of sodium and water, resulting in signs and symptoms of fluid retention, has long

been a hallmark of heart failure. The precise mechanism whereby the heart signals the kidney inthe early stages of heart failure to retain sodium and water is still unknown, although in the late

stages reduced cardiac output and impaired renal blood flow are likely playing a major role.

In early heart failure, when normal cardiac output is maintained by means of compensatory

mechanisms and renal blood flow is not reduced, some sodium retention still occurs. Curiously,some patients with advanced heart failure may not demonstrate peripheral edema or ascites. This

suggests that in some cases, counter-regulatory natriuretic peptides can be acting to maintain

natriuresis. Perhaps release of ANP and BNP in the early stages of heart failure can offset the

tendency to retain sodium. Salt and water retention usually becomes evident in heart failure asperipheral vasoconstriction occurs in the face of a falling cardiac output. This is associated with

activation of the RAAS. Angiotensin II preserves glomerular filtration rate in patients with heartfailure even when renal perfusion is severely compromised, independent of its propensity to

support systemic blood pressure.135

Intraglomerular hydraulic pressure and therefore glomerularfiltration are preserved by the constriction of glomerular efferent arterioles through angiotensin

II.136

Increased intrarenal formation of angiotensin II during a reduction in renal artery pressure

maintains efferent arteriolar tone and, consequently, the effective filtration pressure.137

Theresulting high level of filtration fraction favors changes in the postglomerular circulation that

promote avid proximal fluid reabsorption by means of elevated peritubular capillary oncotic

pressure.136

Increased aldosterone acts principally on the cortical collecting tubules to conserve

sodium, with a concomitant loss of potassium. Because the plasma volume and blood pressurevary considerably from day to day, there is no consistent relation between the RAAS and fluid

retention.

The mechanisms of sodium and water retention in heart failure are multiple and complex (Table

247). Sympathetic nervous system traffic to the kidney favors sodium retention. Increased AVP

activity diminishes free water clearance. The prostaglandins normally dilate afferent glomerulararterioles to enhance intraglomerular flow and pressure, and their inhibition by nonsteroidal

antiinflammatory agents (NSAIDs) can lead to a marked reduction in filtration and sodium

retention. Enhanced sodium reabsorption of heart failure also occurs in the ascending loop ofHenle, as well as in the cortical and medullary collecting ducts. Eventually, plasma volume

expansion occurs, but at the expense of circulatory and tissue congestion.