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(Circulation. 1962;26:12.)
© 1962 American Heart Association, Inc.

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Renal and Adrenal Relationships in Refractory Edema

EDWARD KESSLER M.D.¹; JAMES G. HILTON M.D.¹; M. ROBERT LEVY M.D.¹

¹ From the Medical Service and Medical Research Laboratory, Veterans Administration Hospital, East Orange, New Jersey, and the Department of Medicine, St. Luke's Hospital, New York, New York.

The relationships between the excretion of sodium and water and adrenal activity in patients with refractory edema have been investigated.

Experiments have been performed over a prolonged period with varying doses and combinations of spironolactone, prednisone, hydrochlorothiazide, Su4885, and ACTH. In four patients with Laennec's cirrhosis with ascites the effects of prednisone on the excretion of water and solute were studied during maximum water diuresis.

The results indicate that diuretic agents may increase the excretion of sodium without water within certain undefined limits. This effect probably resulted from the delivery to the concentrating segment of an amount of sodium inadequate to dissipate the gradients favoring water reabsorption.

Prednisone appeared to have a dual effect: one on the excretion of water, the other on the excretion of sodium. The effects on sodium and water did not appear to be related.

The effects of prednisone on the excretion of water support the concept that the glucocorticoids exert an effect on water in the renal tubules rather than on the posterior pituitary.

Prednisone enhanced sodium excretion only when given together with another diuretic agent. It is suggested that the failure of prednisone alone to increase sodium excretion resulted from a blockade of ACTH secretion and, thereby, the adrenal synthetic pathway of aldosterone, whereas the renal aldosterone-stimulating pathway continued to function. The potentiating effect of prednisone on the excretion of sodium becomes apparent only when aldosterone activity is overcome in the renal tubules by the natriuretic effects of various diuretics.

It is considered possible that renal aldosterone-stimulating hormone acts only under more intense stimuli to edema formation.