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 in the 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 as peripheral 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 heart failure even when renal perfusion is severely compromised, independent of its propensity to support systemic blood pressure.135 Intraglomerular hydraulic pressure and therefore glomerular filtration 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 The resulting 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 pressure vary 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 glomerular arterioles 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 of Henle, as well as in the cortical and medullary collecting ducts. Eventually, plasma volume expansion occurs, but at the expense of circulatory and tissue congestion.