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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
RENAL SODIUM LOSS IN BRONCHOGENIC CARCINOMA. JAMA. 1962;182(2):185–186. doi:10.1001/jama.1962.03050410081019
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