The renal and cardiovascular systems are closely interdependent. Two main pathophysiological forces account for secondary renal dysfunction in heart failure:
Decreased renal blood flow in advanced heart failure, marked vasoconstriction of the afferent arteriole depresses the glomerular filtration rate.
Increasing neurohumoral activation, as disease increases in severity, the protective vasodilatation and natriuresis induced by increased levels of atrial natriuretic peptide (ANP) are overwhelmed by the vasoconstriction and salt and water retention induced by increasing activation of the sympathetic nervous system and renin-angiotensin-aldosterone axis.
Conversely, left ventricular dysfunction and heart failure are common complications of chronic renal failure, via several mechanisms:
Volume overload. Loss of renal function leads to salt and fluid retention. Other contributory factors are chronic anemia and an arteriovenous access fistula.
Pressure overload. Systemic hypertension and decreased aortic and large artery compliance place an excessive afterload burden on the dysfunctional heart.
Negative inotropism. Hypoxemia, subendocardial ischemia, certain buffers added to hemodialysis fluid, elevated parathyroid hormone, and uremic toxins all depress myocardial contractility.
Various studies have addressed the prognostic implications of renal insufficiency in heart failure. A retrospective analysis of renal dysfunction (creatinine >2 mg/dL) was recently conducted in participants in the Studies Of Left Ventricular Dysfunction (SOLVD).
The criteria for randomization to the angiotensin-converting enzyme (ACE) inhibitor enalapril or placebo were an ejection fraction <35% and New York Heart Association (NYHA) functional class II-III. The end points of the analysis were pump failure death, allcause mortality, and hospitalization for heart failure. The results indicated that even moderate renal insufficiency was independently associated with an increased risk of all three end points, hence of heart failure progression. The presumed mechanism is that renal dysfunction induces salt and water retention, increases cardiac filling pressures, and causes progressive ventricular dilatation. Another recent study in severe heart failure added further important observations: renal function was more closely associated with mortality in severe heart failure than other established risk factors, including NYHA class and left ventricular ejection fraction. In addition, renal function correlated significantly, and more closely than left ventricular ejection fraction, with plasma neurohormones (in particular, N-terminal ANP). Renal function is thus one of the most important determinants of prognosis in early and advanced heart failure and a more potent discriminator of risk than cardiac parameters such as left ventricular ejection fraction. The data also suggest that, rather than simply being a marker of the severity of underlying disease, the adequacy of renal function may be a primary determinant of compensation in heart failure. Hence, interventions that improve renal function may delay disease progression. Diuretic therapy is therefore an essential symptomatic treatment for fluid overload expressed as pulmonary congestion or peripheral edema. [gallery ids=""]
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