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October 13, 1962


JAMA. 1962;182(2):185-186. doi:10.1001/jama.1962.03050410081019

The occurrence of renal sodium loss in pulmonary diseases has aroused interest in the basic mechanism of sodium excretion and conservation, apart from the extraneous influences of profuse sweating, diarrhea, and exudation. In a detailed report of bronchogenic carcinoma Ivy1 suggested that inappropriate secretion of antidiuretic hormone (ADH) was a possible cause of renal sodium loss. Certain aspects were discussed in the light of previous reports on the subject by Winkler and Crankshaw (1938), Schwartz and associates (1957), and Roberts (1959), and others.

In addition, Ivy noted in his presentation of data mental aberrations, dizziness, hypotension, the inability to perspire, and urinary retention without obstruction. He suggested that these later phenomena were associated with autonomic neuropathy. It was interesting that the ability to conserve sodium was not present initially when sodium loading resulted in only minimum elevation of the serum sodium. The laboratory data obtained during later phases of

Ivy, H. K.:  Renal Sodium Loss and Bronchogenic Carcinoma ,  Arch Intern Med 108:47-55 ( (July) ) 1961.Crossref
Bartter, F. C., et al.:  Studies on Control and Physiologic Action of Aldosterone , in  Recent Progress in Hormone Research , New York City: Academic Press, Inc., vol. 15, 1959, p. 328.