Electrolyte partition in patients with edema of various origins:☆

Abstract 

Data have been collected on electrolyte partitions in urine of patients with (1) congestive heart failure, (2) hepatic cirrhosis and (3) nephrosis, for the purpose of demonstrating renal function in fluid retention associated with these entities.

Clearance evaluation of sodium and chloride in cardiac decompensation and in normal subjects showed a decrease in sodium clearance with respect to chloride in the cardiac group. Comparison of sodium to chloride in milliequivalent ratios showed a constant decrease in sodium excretion and a depression in the sodium-chloride ratio. This depression varied directly with the severity of the disease process and the degree of fluid retention. These findings are compatible with the hypothesis that edema is a result of retention of sodium by the renal tubules rather than of increased venous pressure.

Patients with hepatic cirrhosis were found to release greatly reduced amounts of sodium; several showed only traces. In this group, the sodium-chloride ratio was even more sharply reduced than in the cardiac group. Such evidence of pathological physiology in the kidney is difficult to reconcile with the widely held theory that fluid retention in cirrhosis is inversely proportional to the plasma albumin concentration.

No disturbance in the normal sodium-chloride ratio could be found in nine patients with nephrosis.

It was concluded that fluid retention in cardiac decompensation and in hepatic cirrhosis is not due solely to increased hydrostatic and decreased oncotic pressure, respectively, but to disturbances of electrolyte metabolism intimately associated with the renal tubules.

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