Primary aldosteronism may be the cause of approximately 10% of the cases of essential hypertension. In approximately 80% of cases, it is caused by an aldosterone secreting adenoma in one adrenal gland, which is called Conn syndrome. The diagnosis of this disorder is important because it is a curable form of hypertension.

The syndrome of primary aldosteronism consists of:

  • Hypertension
  • Hypokalemia
  • Suppressed plasma renin activity
  • Increased aldosterone excretion

Primary aldosteronism is most commonly diagnosed in middle-aged adults and is more common in women than in men. Symptoms include tiredness, muscle weakness, thirst, polyuria and nocturia. The coexistence of hypertension and hypokalemia predicts primary hyperaldosteronism in 50% of cases. Some patients may have normal potassium levels; therefore, normokalemia does not exclude the diagnosis of primary aldosteronism.

The best screening tests are the paired measurements of plasma renin activity and plasma aldosterone concentration. The principle underlying this test is that as aldosterone secretion increases, plasma renin activity should decrease because of sodium retention. Plasma aldosterone concentration is typically >200 ng/L (>20 ng/dL), whereas the plasma renin activity is low. A plasma aldosterone (ng/dL) to plasma renin activity (ng/mL/h) ratio of 20 or more (measured while the patient is upright) supports the diagnosis of an aldosterone-producing tumor. If plasma aldosterone and plasma renin activity are increased and the ratio is </=10, the patient should be investigated for secondary causes of hyperaldosteronism, which include renovascular hypertension, diuretic use, renin secreting tumor, malignant phase hypertension, and coarctation of the aorta. If both aldosterone and renin are depressed, other adrenal and metabolic disorders should be considered.


Beta blockers and calcium channel blockers may interfere with the diagnostic reliability of the aldosterone to plasma renin ratio. They should be withheld for two weeks prior to testing. Spironolactone and loop diuretics induce secondary hyperaldosteronism and should be withheld for 6 weeks before testing. Diltiazem does not interfere and can be used to control blood pressure during testing.

After a positive screening test is obtained, autonomous aldosterone secretion should be confirmed with either a saline infusion test or a 24-hour urine aldosterone excretion during oral salt loading. The principle of these tests is that failure to suppress aldosterone excretion with intravascular volume expansion indicates autonomous aldosterone production. The saline infusion test is performed by administering 2 liters of isotonic saline over 4 hours and then measuring plasma aldosterone. A plasma aldosterone level greater than 10 ng/dL (277.4 pmol/L) is diagnostic of primary hyperaldosteronism, while a level between 5 and 10 ng/dL is considered borderline.

The oral salt loading test is performed by having the patient ingest 12 gram sodium chloride tablets for 3 days and then measuring 24-hour urinary aldosterone. A urinary aldosterone excretion value greater than 12 ug/day (27.7 to 38.8 nmol/day) with urine sodium greater than 250 mEq/24 hours confirms the diagnosis of primary hyperaldosteronism.A 24-hour urinary aldosterone less than 8 ug/d excludes the diagnosis.

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