Primary aldosteronism (primary hyperaldosteronism)

Primary aldosteronism (aka primary hyperaldosteronism) is a condition in which too much aldosterone is produced by the adrenal glands. Its prevalence is unknown, but some studies suggest that it may be present in 5-12% of hypertensive patients.

Aldosterone acts on the distal convoluted tube and collecting duct retaining sodium and water and eliminating potassium in the process.


The classic findings are hypertension and hypokalemia (although the potassium may be normal).

Patients are often asymptomatic hypertensives. Symptoms, when present, may be due to hypokalemia (e.g. muscle weakness).

Metabolic alkalosis, mild hypernatremia and hypomagnesemia may also be present.


Patients that should be tested for primary aldosteronism include hypertensive patients with one or more of the following features: resistant hypertension (hypertension that does not improve with three drugs), adrenal mass, early onset hypertension, or those with family history of primary aldosteronism.

Plasma renin activity (PRA) or plasma renin concentration (PRC) should be obtained (measured on the morning, at 8am). Plasma aldosterone concentration (PAC) may also be obtained and the PAC/PRA ratio may be calculated.

In primary aldosteronism, PRA will be suppressed, PAC elevated and a PAC/PRA ratio will be elevated (>30). Secondary hyperaldosteronism from renal causes will have PRA and PAC elevated with a lower PAC/PRA ratio.

After obtaining an elevated PAC/PRA ratio it is important to obtain proof of aldosterone hypersecretion before establishing the diagnosis (except in patients with unexplained hypokalemia, undetectable PRA or PRC and PAC >20ng/dL). Tests that help to confirm aldosterone hypersecretion include oral sodium loading (5g sodium diet for three days and measurement of 24h urine sodium, aldosterone and creatinine after), saline infusion test, fludrocortisone suppression and captopril challenge.

After that, imaging should be obtained (adrenal CT scan) to determine if disease is unilateral or bilateral.
Around 60% of the cases are bilateral (idiopathic hyperplasia), with the other 40% being unilateral (secreting adenomas).

Adrenal venous sampling may be useful (particularly in patients >35 with unilateral mass, patients with bilateral mass or patients with no mass but high suspicion) to determine if there is lateralization in patients with apparent bilateral disease. If lateralization is present, surgery may be considered even in patients with bilateral disease.


Unilateral or bilateral hyperaldosteronism may be treated differently, regardless of common goals such as normalization of potassium and blood pressure.

Unilateral secretive adenomas may be treated with unilateral adrenalectomy (preferentially with laparoscopic approach). Before the surgery, mineralocorticoid antagonists (spironolactone (ALDACTONE) 12.5-225mg/day or eplerenone (INSPRA) 25-300mg/day divided in two doses) may be useful to reduce the blood pressure and treat hyperkalemia.

After surgery, aldosterone should be measured and potassium supplements, mineralocorticoid antagonists or potassium sparing diuretics should be reduced or suspended.

Patients with bilateral hypersecretion or with unilateral disease that do not want surgery may be treated with medications alone (partial adrenalectomy usually does not work). Spironolactone is the drug of choice in such patients. If that does not work, it may be replaced by eplerenone. Alternatives include other potassium sparing diuretics such as amiloride (MIDAMOR, 5-20mg qDay) or triamterene (DYRENIUM, 100-300mg in two divided doses).


  1. Funder JW et al. The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab (2016) 101 (5): 1889-1916.
  2. Fagugli RM, Taglioni C. Changes in the Perceived Epidemiology of Primary Hyperaldosteronism. International Journal of Hypertension. Volume 2011 (2011).
  3. Rossi GP et al. An Expert Consensus Statement on Use of Adrenal Vein Sampling for the Subtyping of Primary Aldosteronism. Hypertension. 2014;63:151-160.
  4. Young WF. Primary aldosteronism: renaissance of a syndrome. Clinical Endocrinology. Volume 66, Issue 5. May 2007 Pages 607–618.