Chromatographic Separation of the Sodium-Retaining Corticoid From the Urine of Children With Nephrosis, Compared With Observations on Normal Children 12

Observations on the Sodium-Retaining Corticoid in the Urine of Children and Adults in Relation to Sodium Balance and Edema1

“…Chromatographic behavior of the sodium-retaining corticoid: When urine extracts from children with nephrosis were chromatographed on paper, sodium-retaining activity was concentrated in a fraction which moved near cortisone in the toluene and propylene glycol system (14). In the benzene and aqueous methanol system, the activity was associated with a corticosteroid whose lower mobility allowed its separation from cortisone.…”

“…The same fraction contains the activity observed in lipemic nephrosis, in cardiac failure, and in hepatic cirrhosis, As well as in normal men on a diet low in sodium. In children with lipemic nephrosis, this active fraction has been found to contain a corticosteroid resembling aldosterone in a number of physical and chemical properties and in its ability to increase sodium reabsorption by the renal tubules (14,15).…”

“…'A material which increases the output of sodium in the bioassay has been observed in the hydrocortisone fraction (14). When this material was eliminated by chromatography from the fraction in which sodium-retaining activity was sought, the latter fraction did not gain in sodium-retaining activity, as if an interfering substance had been removed; but the diuretic activity found in the urine extracts of some normal adults was reduced or eliminated ( Figure 4).…”

“…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)(15)(16).…”

On the Role of the Kidney during Nephrotic Edema: Potassium Excretion and Sodium Retention 1

“…With predominant emphasis on sodium reabsorption, renal removal of an infused sodium plus non-reabsorbable anion load would obligate excessive potassium excretion. But why should such a hormone be elaborated in the nephrotic syndrome or by individuals on low sodium diets (41) ? Further, a predominant effect on sodium reabsorption would not explain excessive potassium excretion during sodium diuresis, unless anion excretion was the primary determinant of urine composition during diuresis.…”