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Brown JM, et al. The Unrecognized Prevalence of Primary Aldosteronism: A Cross-sectional Study. Ann Intern Med. 2020;173:10-20. PMID 32449886

One-paragraph summary

Across four US academic medical centres, 1,015 participants — 289 normotensive, 115 with stage 1 hypertension, 203 with stage 2, and 408 with resistant hypertension — underwent an oral sodium suppression test regardless of their aldosterone or renin levels, inverting the usual sequence in which a screening aldosterone-renin ratio gates confirmatory testing. Urinary aldosterone was measured in participants in high sodium balance with suppressed renin activity, and biochemically overt primary aldosteronism was defined as urinary aldosterone above 12 μg/24 h. Every blood-pressure category showed a continuum of renin-independent aldosterone production whose severity tracked blood pressure, kaliuresis and lower serum potassium. Adjusted mean urinary aldosterone rose from 6.5 μg/24 h (95% CI 5.2–7.7) in normotension to 14.6 (12.9–16.2) in resistant hypertension, and adjusted prevalence of biochemically overt primary aldosteronism was 11.3% (5.9–16.8), 15.7% (8.6–22.9), 21.6% (16.1–27.0) and 22.0% (17.2–26.8) across the four groups. The aldosterone-renin ratio had poor sensitivity and poor negative predictive value for detecting it.

Key findings

  • Biochemically overt primary aldosteronism in 11.3% of normotensive people — the finding that changes the framing of the whole category.
  • Prevalence rises with hypertension stage but is already substantial at stage 1 (15.7%).
  • Renin-independent aldosterone production is a continuum, not a dichotomy; the diagnostic threshold is a convention imposed on it.
  • The conventional screening test, the aldosterone-renin ratio, misses much of what confirmatory testing finds.
  • The authors state explicitly that these findings "redefine the primary aldosteronism syndrome and implicate it in the pathogenesis of 'essential' hypertension".

Limitations

  • Prevalence estimates rely on arbitrary and conventional diagnostic thresholds applied to a continuous variable — the authors say so.
  • Participants were recruited at four academic medical centres and may not represent the general population; the resistant-hypertension group in particular is a referral population.
  • Oral sodium suppression testing is demanding and was performed under research conditions; its performance in routine care is unknown.
  • Cross-sectional design cannot establish that the biochemical phenotype causes the hypertension, only that they covary.
  • Whether treating people identified this way improves outcomes was not tested, and still has not been (see NCT07727252 in clinical trials landscape).

Why it matters

If a fifth of stage 2 and resistant hypertension — and a tenth of normotension — carries biochemically overt renin-independent aldosteronism, then a large share of what is called "essential" hypertension has an identifiable, specifically treatable mechanism, and screening policies keyed to resistant hypertension miss most of it. The 2025 Endocrine Society guideline's suggestion that everyone with hypertension be screened (PMID 40658480) is a direct descendant. The complementary finding that medically treated primary aldosteronism retains excess cardiovascular risk unless renin is allowed to rise (PMID 29129576) makes the diagnosis actionable rather than merely interesting.

Cited by wiki pages

  • overview
  • secondary hypertension
  • pathophysiology
  • resistant and refractory hypertension
  • guidelines
  • red flags and safety concerns