THE CLINICAL features of primary aldosteronism with hypokalemia have been well established since their first description in 1955.1,2 More recently, Conn and his colleagues 3-6 have proposed additional criteria for the diagnosis of primary aldosteronism in patients who do not exhibit hypokalemia—even during the ingestion of a normal dietary intake of sodium chloride. With the exception of normokalemia, these patients appear to manifest many of the usual clinical features of hypokalemic primary aldosteronism: diastolic hypertension without peripheral edema, increased urinary aldosterone excretion, normal values for the urinary excretion of 17-hydroxy and 17ketosteroids, impaired carbohydrate tolerance, and a "suppressed" response of plasma renin activity to the induction of extracellular volume contraction via dietary salt restriction, the administration of diuretic drugs, or the assumption and maintenance of an ambulatory upright posture. The recognition of this disorder has achieved great practical significance since those same investigators 3-6 have also suggested that
Gunnells JC, Bath NM, Sode J, Robinson RR. Primary Aldosteronism. Arch Intern Med. 1967;120(5):568–574. doi:10.1001/archinte.1967.00300040052009
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