Aldosterone Levels Defining Hypoaldosteronism
Hypoaldosteronism is diagnosed when plasma aldosterone levels are suppressed below 5.4-21.6 ng/dL in the context of appropriate stimulation (such as furosemide-posture challenge), though some cases may show levels as low as 4 ng/dL. 1, 2
Diagnostic Aldosterone Thresholds
Suppressed Aldosterone Ranges
- Aldosterone levels of 5.4 to 21.6 ng/dL have been documented in confirmed hyporeninemic hypoaldosteronism cases when measured after furosemide-posture stimulation testing 1
- Aldosterone levels as low as 4 ng/dL have been reported in aldosterone synthase deficiency, representing severe hypoaldosteronism 2
- The key diagnostic feature is inappropriately low aldosterone relative to the clinical context (hyperkalemia, hyponatremia, elevated renin), rather than an absolute threshold alone 3, 1
Context-Dependent Interpretation
- In neonates and infants with aldosterone deficiency, paradoxically high or normal aldosterone levels may initially be present despite true aldosterone insufficiency, which can mislead diagnosis toward pseudohypoaldosteronism 4
- The diagnosis requires correlation with plasma renin activity, which is typically elevated (>5 ng/mL/hr in adults, >11,400 microU/mL in severe cases) in true hypoaldosteronism 1, 2
Clinical and Laboratory Features
Associated Electrolyte Abnormalities
- Hyperkalemia (K+ >5.3 mEq/L) is present in 94.6% of hypoaldosteronism cases 3
- Hypovolemic hyponatremia occurs in 54.5% of cases, with serum sodium averaging 132.1 ± 6.3 mmol/L 3
- Metabolic acidosis (low bicarbonate, averaging 22.6 ± 3.3 mmol/L) is present in 60.3% of cases 3, 5
Patient Demographics and Risk Factors
- Hypoaldosteronism predominantly affects older adults (median age 77 years) with diabetes mellitus and/or nephropathy 3, 5
- The condition is primarily acquired and isolated (only 5% have concurrent primary adrenal insufficiency) 3
- Mild to moderate renal impairment is commonly present 5, 1
Diagnostic Pitfalls to Avoid
- Do not rely on a single aldosterone measurement—stimulation testing (furosemide-posture challenge or ACTH stimulation) is essential to demonstrate inadequate aldosterone response 1
- In infants, elevated aldosterone does not exclude aldosterone deficiency—genetic testing for CYP11B2 mutations may be necessary when clinical features suggest hypoaldosteronism despite high aldosterone levels 4
- Consider medication effects—prostaglandin inhibitors (indomethacin, ibuprofen), beta-blockers, and ACE inhibitors can suppress the renin-angiotensin-aldosterone axis and mimic or worsen hypoaldosteronism 5, 1
- Distinguish from pseudohypoaldosteronism—in true hypoaldosteronism, fludrocortisone therapy corrects hyperkalemia and acidosis, whereas mineralocorticoid resistance does not respond 5, 1