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).
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.
Absolute Event Rate: 2.9% vs 1.5%
p-value: p=0.01
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=2.91.1 -6.4 vs 1.50.6-2.9 ng/dl; p=0.01); δrelPAC did not differ (13.73.8-25.2% vs 18.49.4-28.0%; 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; 1.20.5-2.2 vs 2.5-0.1-6.2 ng/dl; p<0.001); of note, δrelPAC did not differ (17.18.1-26.8% 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.
Marangon et al. (Fri,) conducted a 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).