Abstract
The kidneys participate to a major extent in the pathogenesis of congestive heart failure. When the heart fails as a pump, a complex alteration of homeostatic mechanisms results. Among the adjustments that occur are changes in the hemodynamic and hormonal mechanisms that regulate the volume and tonicity of the extracellular fluid so that the ability of the kidneys to excrete salt and water is reduced.1 Retention of sodium chloride and water expands the volume of the extracellular fluid, which, in turn, may produce circulatory congestion and edema. This article is a review of some of the physiologic alterations that participate . . .
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