Relation to Sodium Balance

Patients with lipemic nephrosis, cardiac failure, and hepatic cirrhosis frequently accumulate an excess of extracellular fluid, distributed in a pattern characteristic of the underlying disease. These patients commonly have a marked impairment of sodium excretion, while glomerular filtration may be low, normal, or even increased (1-4). This impairment of sodium excretion suggested the presence of a stimulus to tubular reabsorption of sodium, such-as a sodium-retaining hormone with an action like desoxycorticosterone. Since the chemical nature -of the hormone was unknown, a biologic assay was used to measure the sodium-retaining activity of lipid extracts of human urine. Unusually high sodium-retaining activity was present in the urine of some edematous patients with cardiac and renal disease (5). In lipemic nephrosis, this increased sodium-retaining activity was reduced when diuresis followed the use of cortisone, corticotrophin, or concentrated human serum albumin (6, 7). Other observers, using similar methods, have also found abnormal sodium-retaining activity in the urine of patients with nephrosis, heart failure, cirrhosis, and toxemia of pregnancy with edema (812). When extracts of urine from patients with lipemic nephrosis were fractionated by chromatography, the sodium-retaining activity was found to be more polar than desoxycorticosterone (13) and to be concentrated in one fraction which closely resembles aldosterone (14-16). The present report summarizes our results with material extracted by chloroform within 40 minutes after acidification of urine to pH 1.0.