Treatment Guideline Chart
Hyperaldosteronism is a group of disorders in which aldosterone production is inappropriately high, relatively autonomous & non-suppressible by sodium loading.
Signs & symptoms are nonspecific.
Symptoms are caused by hypertension (eg headache), hypokalemia (eg polyuria, nocturia, muscle cramps & weakness, tetany, paralysis, etc) & metabolic alkalosis.

Hyperaldosteronism Diagnosis


  • Correct hypokalemia before performing diagnostic studies

Laboratory Tests

Plasma Aldosterone Concentration/Plasma Renin Activity (PAC/PRA) or Aldosterone:Renin Ratio (ARR)

  • Reliable means of identifying patients with primary hyperaldosteronism and patients whose hypertension may be treatable with Spironolactone
  • Controversy over whether antihypertensives should be stopped prior to Aldosterone:Renin ratio tests
  • An ARR ≥25 when plasma aldosterone level is ≥15 ng/dL suggests hyperaldosteronism

Definitive Test

Definitive Biochemical Diagnosis

  • Stop antihypertensives or agents for ≥4 weeks prior to diagnostic tests (eg Spironolactone, Eplerenone, Amiloride, Triamterene, potassium-wasting diuretics, products derived from licorice root)
    • Medications that are less likely to affect renin and aldosterone measurements (eg Verapamil slow-release, Hydralazine, Doxazosin, Terazosin, Guanethidine or Prazosin) may be used in patients who are not on antihypertensive medication
  • Controversy whether definitive biochemical diagnosis is necessary

Diagnostic Tests

  • High rate of urinary aldosterone excretion with diet high in sodium chloride (NaCl) [eg 12.8 g NaCl or 5000 mg of sodium (Na) x 3 days]
    • Urinary aldosterone excretion rate <10 mcg/24 hours after Na load rules out primary aldosteronism (except glucocorticoid-remediable type); essential hypertension is likely


  • High plasma aldosterone level after intravenous (IV) infusion of NS [eg 2 L of 0.9% NaCl continuous IV given over 4 hours (from 8 am - 12 noon)]
    • Postinfusion plasma aldosterone levels of <5 ng/dL make primary aldosteronism unlikely, while levels >10 ng/dL are a very probable sign of primary aldosteronism

Followed By:

  • Low plasma renin activity with low Na consumption (<40 mg/day) or use of diuretic [eg Furosemide 120 mg per orem (PO) in divided doses] suggests diagnosis of primary aldosteronism


  • Patients with the following should receive evaluation for hyperaldosteronism:
    • Sustained hypertension (≥150 mmHg systolic or ≥100 mmHg diastolic)
    • Hypertensive patient with spontaneous or profound diuretic-induced hypokalemia
    • Untreated hypertension with low serum K+ levels (~3.5 mmol/L)
    • Refractory hypertension or patients receiving ≥3 antihypertensives
    • High risk for aldosteronism (resistant hypertension or incidental imaging of abnormal adrenal gland)
    • Family history of early-onset hypertension or cerebrovascular accident (CVA) at a young age (<40 years old)
    • Hypertensive 1st-degree relatives of patients with primary aldosteronism


Magnetic Resonance Imaging/Computed Tomography (MRI/CT) scan

  • MRI or CT of adrenal glands to diagnose adrenal adenomata
    • MRI is not more sensitive than CT

Adrenal Venous Sampling

  • Adrenal vein catheterization should only be performed by an experienced radiologist
  • Aids imaging studies in determining whether any adrenal masses or nodules represent adenoma or hyperplasia
  • Samples of adrenal venous blood are taken for the measurement of aldosterone and cortisol from the adrenal venous effluent and from the inferior vena cava
  • Distinguishes between unilateral and bilateral adrenal disease when surgery can be done and is desired by patient
    • Unilateral adrenal hyperplasia can be determined by unilateral excess of aldosterone secretion which usually indicates presence of aldosteronoma
    • In patients with bilateral adrenal disease, consider genetic testing for glucocorticoid-remediable aldosteronism if they have confirmed primary aldosteronism with family history of aldosteronism or of strokes at <40 years of age, or with hypertension starting at <20 years of age
  • Adrenal venous sampling may not be needed in patients age <35 years with spontaneous hypokalemia, marked excess aldosterone, and unilateral adrenal lesions with features found in radiography consistent with a cortical adenoma on adrenal CT scan
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