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Primary hyperaldosteronism is usually diagnosed when a patient with hypertension has unexplained hypokalemia or when a patient has resistant hypertension.


  1. Etiology

    1. Results from an idiopathic bilateral adrenal hyperplasia in most patients (60–65%)

    2. Results from unilateral aldosterone-producing adenoma in 30–40% of cases (Conn syndrome)

    3. Rarer causes include microadenomas, unilateral adrenal hyperplasia, and adrenal carcinoma.

  2. The overall prevalence, based on community cohorts, is about 5–10%.

    1. Found in 17–23% of patients with resistant hypertension

    2. Prevalence of 34% in patients newly diagnosed with hypertension and obstructive sleep apnea who were referred to a tertiary care center

  3. Pathophysiology

    1. High aldosterone levels lead to salt and water retention and potassium wasting.

    2. Because aldosterone is being produced autonomously, it is not suppressed by volume expansion, as it is normally.

    3. Volume expansion suppresses plasma renin levels.

  4. Most patients have a normal potassium level; 48% of those with aldosterone-producing adenomas and 17% of those with bilateral adrenal hyperplasia are hypokalemic.

    image A normal potassium level does not rule out hyperaldosteronism.


  1. The Endocrine Society recommends screening for primary hyperaldosteronism in patients with the following:

    1. Sustained BP > 150/100 mm Hg

    2. Resistant hypertension

    3. Hypertension and spontaneous or diuretic-induced hypokalemia

    4. Hypertension and sleep apnea

    5. An adrenal incidentaloma

    6. A family history of early-onset hypertension

    7. Cerebrovascular accident at < 40 years of age

  2. There are 3 steps in the diagnosis of primary hyperaldosteronism: screening, confirmatory testing, and determining the subtype.

    1. The plasma aldosterone concentration/plasma renin activity ratio (ARR) is the most commonly used screening test; since patients with primary hyperaldosteronism have elevated levels of aldosterone and suppressed renin levels, the ratio should be elevated.

      1. The ARR can be affected by potassium status, dietary sodium, medications, and age.

      2. Ideally, prior to measurement, the patient should have a normal potassium level and liberal sodium intake.

      3. Medications that minimally affect aldosterone levels include verapamil, hydralazine, and alpha-adrenergic blockers; other antihypertensive medications and NSAIDs should be stopped for 2–4 weeks when possible.

      4. The optimal cut point is unclear; a ratio > 20–30 is generally considered a positive test.

      5. Sensitivity ranges from 73% to 87%, with a specificity of about 75%.

    2. If the ARR is abnormal, the patient should be referred to an endocrinologist for confirmatory testing (oral sodium loading, saline infusion, fludrocortisone suppression, or captopril challenge).

    3. Patients with abnormal confirmatory testing should undergo adrenal CT, possibly followed by adrenal vein sampling.


  1. Laparoscopic adrenalectomy should be considered when lateralized aldosterone excess is demonstrated by adrenal vein sampling.

  2. Otherwise, treat with spironolactone (an aldosterone antagonist).

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