RENAL EXCRETION AND TUBULAR REABSORPTION OF SALT IN CUSHING'S SYNDROME AFTER INTRAVENOUS ADMINISTRATION OF HYPERTONIC SODIUM CHLORIDE*

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Abstract
OF THE two mechanisms by which the kidneys regulate the excretion of salt,1 glomerular filtration and tubular reabsorption, changes in the former have been shown to be of importance in the pathogenesis of edema observed in certain patients with congestive heart failure. In such patients, Merrill (1) has shown that markedly reduced glomerular filtration contributes to the abnormal retention of injected sodium chloride observed by Futcher and Schroeder (2). Despite the fact that the rate of glomerular filtration is frequently reduced also in patients with Addison's disease (3), such patients lose salt in the urine to an abnormally great degree. On the basis of this and other evidence, it seems likely that deficiency of adrenal hormones results in a diminished capacity of the renal tubular cells to reabsorb salt. The reverse effect (increased capacity) has not been demonstrated to occur in that form of adrenal hyperfunction which results in Cushing's syndrome. Indeed, Soffer et al. (4) have observed that when desoxycorticosterone acetate (DCA) and salt are administered to patients with Cushing's syndrome, these subjects excrete salt to a greater degree than do normal subjects similarly treated. This investigation was undertaken in order to study tubular reabsorption of salt in patients with Cushing's syndrome. Observations have been made on the influence of an intravenous injection of a large amount of sodium chloride upon the rate of salt excretion, the renal filtration rate and plasma flow in these subjects.