To the Editor:—
It is the purpose of this discussion to emphasize that when the term secondary aldosteronism is used, it should be appreciated that it is the effect of aldosterone which is "secondary" and the quotation marks might be properly placed as in the above title.When it was demonstrated by Deming and Luetscher1 that the urine of some edematous subjects contained a substance which could bring about the retention of sodium by the kidneys of experimental animals to which this substance was administered, and, when this substance was identified by Simpson and Tait2 as the adrenal hormone, aldosterone, it appeared that a straightforward explanation for such edema might be provided by invoking the excessive production of aldosterone as the causative agent. The appellation "secondary aldosteronism" came into being and was applied inclusively to all the edematous states in which an increased excretion of aldosterone could be
Gwinup G, Hamwi GJ. "Secondary" Aldosteronism. JAMA. 1965;191(11):951–952. doi:10.1001/jama.1965.03080110075040
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