ECEESPE2025 Rapid Communications Rapid Communications 1: Adrenal and Cardiovascular Endocrinology (5 abstracts)
Role of postural test in differentiating from primary aldosteronism to low-renin hypertension
Irene Tizianel 1,2 , Elena Pagin 1,2 , Eugenio Ragazzi 3 , Alberto Madinelli 1,2 , Simona Censi 1,2 , Chiara Sabbadin 1,2 , Franco Mantero 2 , Caterina Mian 1,2 , Mattia Barbot 1,2 , Giorgia Antonelli 2,4 & Filippo Ceccato 1,2
1Endocrine Disease Unit, University Hospital of Padova, Italy, Padova, Italy; 2Deparment of Medicine DIMED, University of Padova, Padova, Italy; 3Studium Patavinum, University of Padova, Italy, Padova, Italy; 4Laboratory Medicine Unit, University Hospital of Padova, Italy, Padova, Italy
JOINT1328
Background: The concept of primary aldosteronism (PA) as a categorical disease has recently been revised; instead, PA may be considered as a continuous spectrum of disease, characterized by renin-independent aldosterone excess. The role of confirmatory tests in the diagnostic process of PA is still controversial. Among them, the postural stimulation test (PST) was proposed in the past for PA subtyping, however results were contradictory.
Objective: To assess PST role in differentiating from PA to low-renin hypertension (HTN).
Patients and methods: 190 patients with arterial hypertension and at least one positive aldosterone to renin ratio (ARR) underwent confirmatory tests (saline infusion test and/or captopril challenge test). 80 were confirmed PA and 110 PA were identified as low-renin HTN. Baseline clinical and biochemical data and PST response were assessed. Principal component analysis (PCA), Partial Least Square-Discriminant Analysis (PLS-DA) and K-means clustering network were used to compute an integrated analysis.
Results: PST response showed 56/190 patients (29%) with suppressed renin levels both in clinostatism (clino) and orthostatism (ortho), 56/190 (29%) with desuppression of renin levels from clino to ortho, and 78/190 (42%) with non-suppressed clino renin which remained measurable in ortho. In the category of always suppressed renin 54/56 (92%) patients were PA, while 45/56 (80%) of patients in the category renin from suppressed to measurable were identified as low-renin HTN. Multivariable regression analysis showed increasing K levels (OR 12.5, 95% CI 3.4-42.5, P<0.001) and measurable ortho_renin (OR 351.6, 95% CI 31.35-3921, P<0.001) as significant predictors of low-renin HTN. Cluster analysis was able to distinguish PA from low-renin HTN. Cluster 1 correctly included 57/80 PA and Cluster 2 correctly included 104/110 low-renin HTN. Cluster 1 PA patients showed a higher frequency of suppressed renin levels at baseline and during PST, with a prevalence of clino_reninsuppressed of 100% and a prevalence of ortho_reninsuppressed of 95%. Cluster 1 low-renin HTN patients had lower potassium levels and a higher frequency of suppressed renin levels at diagnosis and during PST, compared to Cluster 2. LS-DA and PCA confirmed that ortho_renin, renin response to PST and presence of hypokalemia were the most accurate parameters to distinguishing PA from low-renin HTN.
Conclusion: PST demonstrated his role in the differential diagnosis of suspected PA, in particular regarding renin response during the test.
Volume 110
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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