Aldosterone, Potassium and Acidosis

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Abstract
In 1957 in the pages of the Journal, Hudson and his colleagues reported the case of a patient with Stokes-Adams attacks and hyperkalemia who also had inappropriately low levels of aldosterone in the urine.1 Since that time at least 30 additional cases of isolated hypoaldosteronism have been reported, including one in the present issue of the Journal (p. 361). The clinical features of this syndrome have varied considerably but except in one case have included hyperkalemia, usually symptomatic, and normal glucocorticoid function, most often established by a normal cortisol or 17-hydroxysteroid response to ACTH administration. In part because of . . .
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