Primary aldosteronism (PA), previously considered a rare cause of hypertension, may be responsible in recent series for 5-10% of the hypertensive population. Although one might consider PA as the main cause of secondary hypertension, caution is recommended when interpreting this sudden "epidemics". Because the classical manifestations of aldosterone excess are not always present, screening for PA must include determinations of random plasma aldosterone: renin ratios (ng/dl:ng/ml/h). Hypertensive patients with ratios > or = 25 (and aldosterone >14ng/dl) must be further investigated with plasma/urine aldosterone suppression tests (IV saline infusion, oral fludrocortisone or high-sodium diets). Failure to suppress is typical of aldosterone autonomy in PA. Differentiation of the two main subgroups (aldosterone-producing adenoma - APA -, and bilateral adrenal hyperplasia or idiopathic hyperaldosteronism - IHA) is mandatory since therapeutic intervention varies. Distinction between APA and IHA is based on the absence of plasma aldosterone increases to renin stimulation (upright posture, diuretics or low-sodium diets) in the first, as opposed to exaggerated responses in the latter. The diagnostic workup must include an adrenal CT and, if necessary, bilateral adrenal vein catheterization and aldosterone measurement to ascertain the source of aldosterone excess.
Hypertension; Mineralocorticoid excess; Hyperaldosteronism; Aldosterone; Plasma renin activity; Potassium
