Key result
Primary aldosteronism linked to ~93% greater absolute PAC drop after captopril challenge vs primary hypertension.
Why the study?
Confirmatory tests for primary aldosteronism assume aldosterone secretion is autonomous from the renin-angiotensin system, but whether post-captopril challenge test aldosterone suppression is truly blunted was unproven.
Does the captopril challenge test demonstrate Angiotensin II-autonomous aldosterone secretion in primary aldosteronism compared to primary hypertension?
Observational (n=719)
No
Does the captopril challenge test demonstrate Angiotensin II-autonomous aldosterone secretion in primary aldosteronism compared to primary hypertension?
The captopril challenge test does not demonstrate Angiotensin II-autonomous aldosterone secretion in primary aldosteronism, challenging its utility as a confirmatory diagnostic test.
Greater aldosterone suppression after captopril in primary aldosteronism challenges test assumptions; leaves confirmatory utility open.
Objective: Confirmatory tests are recommended for the diagnostic workup of primary aldosteronism (PA) in patients with an elevated aldosterone-to-renin ratio. They are based on the presumed autonomy of the adrenal secretion of aldosterone from the renin-angiotensin system in PA: e.g., persistent suppression of renin and production of aldosterone after a captopril challenge test (CCT). We sought to test whether post-CCT aldosterone suppression is blunted in patients with PA due to Angiotensin II-autonomous aldosterone secretion. Design and method: From hypertensive patients who consecutively underwent standardized biochemical screening for secondary causes at our centre, including CCT and after washout from confounding drugs, we identified 643 with a final diagnosis of primary hypertension (PH) and 76 with PA, confirmed by guidelines-defined criteria. Plasma aldosterone concentration (PAC) was measured pre- (PACb) and post-CCT (PACc; sampled 60 minutes after 50 mg of captopril). Absolute and relative changes in PAC (δPAC=PACb-PACc and δrelPAC=(PACb-PACc)/PACb), were compared between patients with PA and patients with PH: 1) matched to PA in a 3:1 ratio by clinically relevant variables (age, sex, BMI, mean blood pressure); 2) in the lowest tertile of renin. Results: When clinically matched, the absolute drop in PAC was larger, not smaller, in PA compared to PH (n=49 and 147, respectively; δPAC=2.9[1.1 -6.4] vs 1.5[0.6-2.9] ng/dl; p=0.01); δrelPAC did not differ (13.7[3.8-25.2]% vs 18.4[9.4-28.0]%; p=0.194). In patients with PH, δPAC and δrelPAC increased with increasing baseline values of renin (p<0.001 for both), as expected. For those in the lowest tertile of renin (<=4.4 mIU/L or <=0.41 ng/ml/h), δPAC was smaller compared to patients with PA (n=212 and 76; 1.2[0.5-2.2] vs 2.5[-0.1-6.2] ng/dl; p<0.001); of note, δrelPAC did not differ (17.1[8.1-26.8]% vs 13.4[-0,5-24.5]%, p=0.174). Conclusions: These results lend no support to the biological premise of an AngII-autonomous aldosterone secretion in PA, nor to the use of CCT as a confirmatory test, accordingly.
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Marangon et al. (2026) conducted an observational in Primary aldosteronism and primary hypertension (n=719). Primary aldosteronism vs. Primary hypertension was evaluated on Absolute drop in plasma aldosterone concentration (δPAC) after captopril challenge test (p=0.01). Primary aldosteronism showed a larger absolute drop in plasma aldosterone concentration after captopril challenge compared to matched primary hypertension (2.9 vs 1.5 ng/dl; p=0.01).
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