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Key Features

Essentials of Diagnosis

  • Hypertension may be severe or drug-resistant

  • Hypokalemia (in minority of patients) may cause polyuria, polydipsia, muscle weakness

  • Low plasma renin; elevated plasma and urine aldosterone levels

General Considerations

  • Excessive aldosterone production

    • Increases sodium retention and suppresses plasma renin

    • Increases renal potassium excretion that can lead to hypokalemia

  • Cardiovascular events are more prevalent in patients with aldosteronism (35%) than in those with essential hypertension (11%)

  • May be caused by

    • An aldosterone-producing adrenal adenoma (Conn syndrome), 40% of which have been found to have somatic mutations in a gene involved with the potassium channel

    • A unilateral adrenal adenoma/hyperplasia or bilateral adrenal hyperplasia

  • Bilateral aldosteronism may be corticosteroid suppressible due to an autosomal-dominant genetic defect allowing ACTH stimulation of aldosterone production

  • Malignant ovarian tumors are rare cause of hyperaldosteronism


  • Accounts for 8–10% of all cases of hypertension and for 20% of cases of resistant hypertension

  • Should also be suspected with early onset hypertension or stroke before age 50 years (or both)

  • Patients of all ages may be affected, but the peak incidence is between 30–60 years

Clinical Findings

Symptoms and Signs

  • Hypertension is typically moderate but may be severe

  • Some patients have only diastolic hypertension, without other symptoms and signs

  • Edema (rare)

  • Muscle weakness (at times with paralysis simulating periodic paralysis), paresthesias with frank tetany, headache, polyuria, and polydipsia may be seen in patients with hypokalemia

Differential Diagnosis

  • Essential hypertension

  • Hypokalemic thyrotoxic periodic paralysis

  • Renal vascular hypertension (hypertension and hypokalemia, but plasma renin activity is high)

  • Hypokalemia due to other cause, eg, diuretics

  • Secondary hyperaldosteronism (dehydration, heart failure)

  • Congenital adrenal hyperplasia: 11β-hydroxylase deficiency, 17α-hydroxylase deficiency

  • Cushing syndrome

  • Excessive real licorice ingestion

  • Syndrome of cortisol resistance


Laboratory Tests

  • Plasma potassium should be determined in hypertensive individuals; however, hypokalemia is present in only 37% of affected patients

  • An elevated serum bicarbonate (HCO3) concentration indicates metabolic alkalosis and is commonly present

  • Testing for primary aldosteronism should be done for all hypertensive patients with any of the following:

    • Sustained hypertension above 150/100 mm Hg on 3 different days

    • Hypertension resistant to three conventional antihypertensive drugs, including a diuretic

    • Controlled blood pressure requiring four or more antihypertensive drugs

    • Hypokalemia, whether spontaneous or diuretic induced

    • Personal or family history of early onset hypertension or CVA at age ≤ 40 years

    • First-degree relative with primary aldosteronism

    • Presence of an adrenal mass

    • Low plasma renin activity

  • Testing protocol

    • For at least 2 weeks prior to testing, patients should

      • Consume a diet high in NaCl (> 6 g/day)

      • Hold certain medications: all diuretics, ACE inhibitors, ARBs (stimulate plasma renin activity [PRA]); β-blockers, clonidine, NSAIDs (suppress PRA), oral estrogens, and oral contraceptives

      • Medications that are allowed include slow-release verapamil, hydralazine, terazosin, ...

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