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December 1959

Studies in Man on Hyper- and Hypoaldosteronism

Author Affiliations

Birmingham, Ala.

From the Department of Medicine and University Hospital, the University of Alabama Medical Center, and the Medical Service Veterans Administration Hospital.; Trainee, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health (Drs. Chenault and McNeill), and Student Fellow, National Institutes of Health (Mr. Nickerson), Bethesda, Md.

AMA Arch Intern Med. 1959;104(6):982-994. doi:10.1001/archinte.1959.00270120138018

Introduction  The classification of clinical disorders associated with an abnormal secretion of aldosterone was clearly outlined by Conn.1 Primary hyperaldosteronism had been previously described by Conn2 and secondary hyperaldosteronism in patients with nephrosis, congestive heart failure, and cirrhosis by Deming, Luetscher, and Curtis.3,4 Although the syndrome of primary hypoaldosteronism had not been described, it was anticipated by Conn,1 and subsequently two patients have been reported as representing examples of this syndrome.5,6 The exact pathophysiology of primary hypoaldosteronism is still in doubt.7Although increased aldosterone secretion is not necessarily the primary cause of sodium and water retention in patients with edema, it is, in general, one constant finding in the chain of events leading to edema formation. Two groups of substances have been used to modify this aspect of edema; inhibitors of adrenal cortical activity8 and peripheral antagonists of aldosterone.9 The therapeutic usefulness of the adrenal inhibitor used most extensively,