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Adrenal-based mineralocorticoid excess that is not secondary to excessive angiotensin II or adrenocorticotrophic hormone (ACTH) exists primarily as primary aldosteronism (PAL) and rarely as deoxycorticosterone-secreting adrenal tumor. The availability and wide application of the plasma aldosterone—plasma renin activity (PRA) ratio as a screening test for PAL has led to the recent recognition that PAL is common, possibly accounting for 5 to 10% of patients with hypertension, with most normokalemic. Detection and appropriate management of PAL relies on (1) screening of all patients with hypertension and not just those with hypokalemia or resistant hypertension; (2) confirmation of PAL using a reliable diagnostic approach such as fludrocortisone suppression testing (saline infusion testing may lack sensitivity); and (3) careful further assessment to differentiate the subtype, including genetic testing for the hybrid gene that causes glucocorticoid-remediable aldosteronism, and adrenal venous sampling to differentiate unilateral from bilateral aldosterone overproduction. The establishment of other underlying genetic mutations and new genetic tests should also aid in the detection of PAL and potentially curable hypertension.
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