Since its initial description in 1955, primary aldosteronism was thought to be a rare cause of hypertension. However, with improved screening methodologies, it appears that primary aldosteronism is the most common form of secondary hypertension. Diagnosis of this disorder results in either the cure of hypertension or targeted pharmacotherapy. In addition, recent evidence suggests that aldosterone excess may have specific cardiotoxicity that is reversible with treatment. Patients with hypertension and hypokalemia and most patients with treatment-resistant hypertension should undergo screening for primary aldosteronism. A random and ambulatory ratio of plasma aldosterone concentration (ng/dl) to plasma renin activity (ng/ml per hour) >20 and a plasma aldosterone concentration >15 ng/dl is a positive screen for primary aldosteronism. A plasma aldosterone concentration/plasma renin activity ratio >20 alone is not diagnostic of primary aldosteronism; primary aldosteronism must be confirmed by demonstrating inappropriate aldosterone secretion with either the intravenous saline suppression test or measurement of 24-hour urinary aldosterone while on a high-sodium diet. The 2 major subtypes of primary aldosteronism are unilateral aldosterone-producing adenoma and bilateral idiopathic hyperplasia. Patients with aldosterone- producing adenoma are usually treated with unilateral adrenalectomy, and patients with idiopathic hyperplasia are treated medically. The subtype evaluation may require one or more tests, the first of which is imaging the adrenals with computed tomography (CT). When CT reveals a solitary unilateral macroadenoma (>1 centimeter) and normal contralateral adrenal morphology in a patient with primary aldosteronism, unilateral laparoscopic adrenalectomy is a reasonable therapeutic option. However, in many cases, CT imaging may reveal normal-appearing adrenals or ambiguous findings. Adrenal venous sampling helps solve these clinical dilemmas.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine