Physiology of Urinary Cortisol Excretion

Publisher Website
Google Scholar
Abstract
The mechanisms leading to the renal excretion of cortisol have been studied over a wide range of plasma cortisol concentrations. In 3 normal adult males with endogenous plasma cortisol suppressed by dexamethasone, cortisol was infused intravenously in successively increasing amounts and simultaneous renal clearances of cortisol and inulin were determined after brief equilibration at each new concentration of plasma cortisol. In other subjects, clearances of endogenous cortisol and creatinine were measured. Urinary cortisol was quantitated by a glass fiber chroma tographic method, plasma cortisol was estimated as Porter-Silber chromogen, and the percentage of protein binding of cortisol in plasma was determined at 37 C using an ultracentrifugation technique. As plasma cortisol was increased stepwise by infusion, there was a progressive decrease in protein binding, an increase in the filtration of unbound cortisol, and linear increases in both the excretion and reabsorption of cortisol. While the mechanism (s) for reabsorption of cortisol by renal tubules remain (s) unknown, these data are consistent with possible glomerular filtration of unbound cortisol followed by passive backdiffusion of most filtered cortisol. If reabsorption of cortisol is an active process, there is no evidence for a tubular maximum with plasma levels up to 121 μg/100 ml. In contrast to the very low renal clearance of endogenous cortisol in normal subjects, the suppressed group subjected to cortisol infusion showed a high, relatively constant rate of cortisol clearance, averaging 54 ml/min, over a wide range of plasma concentrations. These observations lend basic support to the clinical usefulness of urinary “free” cortisol measurements in the diagnosis of chronic glucocorticoid excess.

This publication has 11 references indexed in Scilit: