ArticleHypertension (Dallas, Tex. : 1979)2025
ACE Inhibition to Distinguish Low-Renin Hypertension From Primary Aldosteronism.
Article in Hypertension (Dallas, Tex. : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Race and Ancestry in Primary Aldosteronism.Journal of the American Heart Association · 2026Article
- Prevalence, clinical characteristics and management of low-renin hypertension: a real-world cohort study.Journal of human hypertension · 2026Article
- Renin-Guided Risk Stratification and Therapy in Hypertension to Reduce Major Adverse Cardiovascular Outcomes.medRxiv : the preprint server for health sciences · 2026Article
- Aldosterone and the Broken Clock: Restoring Circadian Blood Pressure Rhythm in Primary Aldosteronism.Journal of the American Heart Association · 2026Article
- Postural test to differentiate primary aldosteronism from low-renin hypertension: a retrospective single-center study.Journal of endocrinological investigation · 2026Article
- NT-proBNP and its association with autonomous aldosterone production in primary aldosteronism.Therapeutic advances in endocrinology and metabolism · 2026Article
- Screening and Diagnosis Trends for Primary Aldosteronism: A Longitudinal Nationwide Cohort Study of 7.8 Million People.medRxiv : the preprint server for health sciences · 2025Article
- Discordance and shortcomings of aldosterone suppression tests in primary aldosteronism.European journal of endocrinology · 2025Article
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7 authors.
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Abstract
backgroundPrimary aldosteronism (PA) is a distinct cause of low-renin hypertension (LRH), characterized by inappropriate aldosterone production. We investigated the distinction between LRH and PA by leveraging the physiological effects of angiotensin-converting enzyme inhibition.
methodsWe conducted a retrospective cohort study including 756 patients with LRH who underwent a captopril challenge test (CCT) for evaluation of PA. The distinction between PA and LRH was assessed using 4 CCT criteria: (1) Post-CCT plasma renin activity <1 ng/mL per hour and plasma aldosterone concentration decrease <30%; (2) Post-CCT aldosterone-to-renin ratio (ARR) >30 ng/dL per ng/mL per hour; (3) Post-CCT plasma renin activity <1 ng/mL per hour; and (4) Post-CCT plasma aldosterone concentration >11 ng/dL. Longitudinal outcomes following aldosterone-targeted therapy were assessed using the Primary Aldosteronism Surgery Outcome and Primary Aldosteronism Medical Outcome criteria.
resultsThere was a continuous spectrum of nonsuppressible aldosterone production post-CCT. When interpreting CCT results based on both renin and aldosterone responses (criteria 1 or 2), 57.8% to 66.3% of patients were classified as having PA. In contrast, when based on aldosterone or renin responses alone (criteria 3 or 4), 82.5% to 95.1% of patients were classified as having PA. Complete or partial treatment response rates following aldosterone-targeted therapy were high, ranging from 86.5% to 91.7%, regardless of CCT interpretation.
conclusionsThese findings highlight the blurred distinction between LRH and PA. Although persistently suppressed renin, or elevated aldosterone, following captopril facilitated the maximum capture of PA cases, the implementation of aldosterone-targeted therapy provided similar benefits to all patints, regardless of CCT interpretation. Empirical aldosterone-directed therapy for patients with LRH suspected of having PA may be an appropriate alternative to laborious diagnostics to confirm PA.
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