hyperaldosteronism

Introduction

Excessive secretion of aldosterone:

Etiology

• primary hyperaldosteronism
  • aldosterone-producing adrenal adenoma
  • bilateral adrenal cortical hyperplasia
    • glucocorticoid-remediable hyperaldosteronism
      • 11-beta hydroxysteroid dehydrogenase deficiency
  • criteria for diagnosis
    • diastolic hypertension without edema
    • hyposecretion of renin that fails to increase during volume depletion (upright posture, sodium depletion)
    • hypersecretion of aldosterone that does not suppress appropriately with volume expansion (salt loading)
• secondary hyperaldosteronism
  • aldosterone often higher than in primary hyperaldosteronism
  • overproduction of renin
    • primary reninism
      • renin-producing juxtaglomerular cell tumor
      • renin-producing tumors may also arise from the ovary
      • Bartter's syndrome
    • decrease in renal blood flow
      • atherosclerosis
      • fibromuscular dysplasia
      • arteriolar nephrosclerosis
  • increased circulating levels of renin substrate (angiotensin-1) in pregnancy
  • licorice abuse

Clinical manifestations

• mild to moderate diastolic hypertension
• headaches
• polyuria
• muscle weakness
• fatigue
• edema may occur with secondary hyperaldosteronism

Laboratory

• serum potassium: hypokalemia
  • hypokalemia inconsistently associated with primary hyperaldosteronism
• serum sodium: hypernatremia
• ABG may show metabolic alkalosis
• urinalysis
  • pH neutral to alkaline
  • specific gravity low
  • urine K+ in a patient with hypokalemia indicates renal K+ losing state
  • urine Cl- often elevated
  • after a 3 day high salt diet
    • 24 hour urine collection
    • measure Na+, K+, creatinine & aldosterone
    • aldosterone > 12 ug & urine Na+ > 200 meq/24 hr confirms diagnosis of hyperaldosteronism
• plasma aldosterone elevated relative to plasma renin activity
  • plasma aldosterone (ng/dL)/plasma renin activity (mg/mL/hr)
    • > 20 suggests primary hyperaldosteronism
      • > 100 may have 100% predictive value
    • < 10 suggests secondary hyperaldosteronism
  • selective venous sampling may help localize tumor
  • discontinue spironolactone or eplerenone 6 weeks prior to testing
• autonomy of aldosterone secretion:
  • salt loading or saline infusion fails to suppress plasma aldosterone
  • captopril suppression test
  • fludrocortisone suppression test
• elevated plasma renin in patients on ACE inhibitor or ARB rules out hyperaldosteronism
• serum cortisol is normal
• see ARUP consult

Diagnostic procedures

• electrocardiogram:
  • left ventricular hypertrophy
  • signs of hypokalemia
    • prolongation of ST segment
    • U waves
    • T-wave inversions
• adrenal vein sampling prior to adrenalectomy

Radiology

• CT scan may demonstrate adrenal mass (see adrenal incidentaloma)
• MRI more sensitive than CT
• iodocholesterol scan may be useful

Management

• unilateral adrenal aldosterone-secreting adenoma
  • adrenalectomy (adrenal vein sampling prior to adrenalectomy)
  • aldosterone antagonis if not surgical candidate
• bilateral adrenal hyperplasia
  • aldosterone antagonists
    • spironolactone 25-100 mg every 8 hours
    • eplerenone
    • triamterene
    • amiloride
  • unilateral or bilateral adrenalectomy seldom cures hypertension
• dietary sodium restriction
• glucocorticoid-remediable hyperaldosteronism
  • dexamethasone has less mineralocorticoid activity than cortisol

More general terms

• adrenal gland disease
• syndrome

More specific terms

• Bartter syndrome
• primary hyperaldosteronism (Conn's syndrome)

Additional terms

• apparent mineralocorticoid excess syndrome
• hypoaldosteronism; mineralocorticoid deficiency

Patient information

hyperaldosteronism patient information