Abstract
Edematous patients with renal sodium and water retention, particularly cardiac failure and cirrhosis, have been suggested to have a decreased "effective blood volume." This enigmatic and undefined term was coined because edematous patients were found to have increased, rather than the earlier proposed decreased, blood volumes. This article discusses the advances that have occurred in understanding the pathophysiology of edema as occurs in conditions such as cardiac failure, cirrhosis, and pregnancy. The regulatory mechanisms that lead to increased sodium and water retention by the normal kidney are related to arterial underfilling, as a result of a decrease in cardiac output, arterial vasodilation, or both.
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