STUDIES IN NEPHROSIS: CHEMICAL CORTICOIDS, SALT-RETAINING FACTOR, AND EFFECT OF ACTH*

Abstract

THE accumulation of edema fluid in patients suffering from the nephrotic syndrome, and the mechanism of its production, have been the subject of considerable speculation and research. According to Barnett (1) who has recently reviewed existing knowledge of the pathogenesis of this type of edema, there is evidence that a glomerular-tubular imbalance exists in the kidney in the nephrotic state. The preponderance of tubular function may depend on relatively decreased glomerular function, due either to pathologic lesions in the glomeruli or to “circulatory insufficiency” secondary to decreased serum osmotic pressure. Alternatively, it may indicate true tubular overfunction in response to excessive stimulation by posterior pituitary antidiuretic hormone, or adrenocortical salt-retaining hormone. The present study was undertaken with the object of further investigating adrenal function in this disease. The excretion of various types of corticoids is only a very indirect measure of adrenocortical function and is subject to error due to technical procedure, conjugation of active compounds, and variations in the pathway of metabolism of the steroids. Nevertheless, a number of different types of determinations have been used in an endeavor to elucidate this problem. The biologically active corticoids which have an action on carbohydrate metabolism may be measured by means of the glycogen deposition test (2).