Postural test to differentiate primary aldosteronism from low-renin hypertension
Irene TizianeliD, Elena PaginiD, Eugenio RagazziiD, Alberto Madinelli, Simona CensiiD, Chiara SabbadiniD, Franco ManteroiD, Caterina MianiD, Mattia BarbotiD, Giorgia AntonelliiD, Filippo CeccatoiD
Abstract
BackgroundThe diagnostic accuracy of screening and confirmatory tests to differentiate primary aldosteronism (PA) among patients with low-renin hypertension (HTN) is suboptimal. We aimed to assess the role of postural stimulation test (PST, previously used for PA subtyping) in differentiating PA from low-renin HTN. Patients and methodsClinical and endocrine data in clinostatic position (CP) and orthostatic position (OP) during PST were evaluated in 190 hypertensive patients: 80 PA and 110 low-renin HTN. Multivariate techniques were computed: Principal Component Analysis (PCA), Partial Least Square-Discriminant Analysis (PLS-DA) and k-means clustering. ResultsPST response differentiated our cohort: 96% of PA were detected in the 56/190 patients with always suppressed renin levels, 80% of patients with low-renin HTN were identified among 56/190 subjects with de-suppression of renin from CP to OP and 78/190 with always measurable renin. Increased potassium and measurable renin in OP were predictors of low-renin HTN. Cluster analysis distinguished PA from low-renin HTN: Cluster 2 included 104/110 low-renin HTN; Cluster 1 PA patients showed a higher frequency of suppressed renin levels at baseline and during PST (100% in CP and 95% in OP, respectively). Cluster 1 low-renin HTN patients had lower potassium and a higher frequency of suppressed renin levels at diagnosis and during PST, compared to Cluster 2. PLS-DA and PCA confirmed that renin in OP, renin response to PST and presence of hypokalemia were the most relevant parameters for distinguishing PA from low-renin HTN. ConclusionRenin response during PST can be used to differentiate PA from low-renin HTN.
02 /Specification & Classification
Click any tag to browse matching papers- Citations
- 0
- Organism
- Assay
- Research Focus
- Approach
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Regulation of Aldosterone Secretion by Substance P and the NK1 Receptor in Aldosterone-Producing Adenomas
A.-G. Lopez, Céline Duparc, … Hervé Lefèbvre·Annales d EndocrinologiePeer-reviewed·Sep 16, 2025
- Renal adaptation to primary aldosteronism requires GDF15 to control plasma potassium level in mice and human.
Justine Billiet, Luciana Morla, … Gilles Crambert·bioRxiv·Oct 22, 2026
- Intrarenal Generation of Aldosterone Contributes to Ischemia-Induced Hypertension and Nephropathy in Mice
Ziwei Fu, Chang‐Jiang Zou, … Tianxin Yang·bioRxiv·Aug 24, 2025
- Modulation of calcium signaling on demand to decipher the molecular mechanisms of primary aldosteronism
Bakhta Fedlaoui, Teresa Cosentino, … Sheerazed Boulkroun·HypertensionPeer-reviewed·Feb 12, 2025
- Zinc transporter somatic gene mutations cause primary aldosteronism
Juilee Rege, Kazutaka Nanba, … William E. Rainey·bioRxiv·Jul 25, 2022
- Renal arterial dysfunction, impaired pressure natriuresis and salt-sensitivity in a mouse model of Cushing syndrome
Hannah M. Costello, Céline Grenier, … Matthew A. Bailey·bioRxiv·Dec 11, 2024