(See also Overview of Adrenal Function.)
Secondary aldosteronism is caused by reduced renal blood flow, which stimulates the renin-angiotensin mechanism with resultant hypersecretion of aldosterone. Causes of reduced renal blood flow include
Secretion may be normal in heart failure, but hepatic blood flow and aldosterone metabolism are reduced, so circulating levels of the hormone are high.
Diagnosis is suspected in patients with hypertension and hypokalemia.
Initial laboratory testing consists of plasma aldosterone levels and plasma renin activity (PRA). Ideally, the patient should not take any drugs that affect the renin-angiotensin system (eg, thiazide diuretics, angiotensin-converting enzyme [ACE] inhibitors, angiotensin antagonists, beta-blockers) for 4 to 6 weeks before tests are done. Elevated aldosterone and plasma renin activity is indicative of secondary aldosteronism. The principal differences between primary and secondary aldosteronism are shown in the table Differential Diagnosis of Aldosteronism.
Differential Diagnosis of Aldosteronism
Treatment involves correcting the cause. Hypertension can usually be controlled with a selective aldosterone blocker such as spironolactone, starting with 50 mg orally once a day and increasing over 1 to 3 months to a maintenance dose, usually around 100 mg once a day. Another potassium-sparing diuretic can be used instead of spironolactone. The more specific drug eplerenone 50 mg orally once a day to 200 mg orally twice a day may be used because, unlike spironolactone, it does not block the androgen receptor (which may result in gynecomastia); it is the drug of choice for long-term treatment in men if low-dose spironolactone is ineffective.
Diagnosis is suspected in hypertensive patients with hypokalemia.
Initial testing includes measurement of plasma aldosterone and plasma renin activity.
Unlike in primary aldosteronism, plasma renin activity is elevated.
Treatment includes correcting the cause.
Hypertension may be controlled with aldosterone antagonists.