cardiorenal connections.docx
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7/29/2019 Cardiorenal Connections.docx
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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.