{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T17:25:03Z","timestamp":1788801903004,"version":"build-2803163510"},"reference-count":23,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2018,7,29]],"date-time":"2018-07-29T00:00:00Z","timestamp":1532822400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Clinical Hypertension"],"published-print":{"date-parts":[[2018,9]]},"abstract":"Angiotensin II<\/jats:styled-content> type\u20101 receptor autoantibodies (AT<\/jats:styled-content>1RA<\/jats:styled-content>b) have been involved in the genesis of primary aldosteronism (PA<\/jats:styled-content>), both in aldosterone\u2010producing adenoma (APA<\/jats:styled-content>) and in idiopathic hyperaldosteronism (IHA<\/jats:styled-content>). In this study, we evaluated the titer of AT<\/jats:styled-content>1RA<\/jats:styled-content>b in 44 PA<\/jats:styled-content> patients (15 with APA<\/jats:styled-content> and 29 with IHA<\/jats:styled-content>) compared with 18 normotensive healthy controls who were matched for gender and age. In 17 PA<\/jats:styled-content> patients (6 APA<\/jats:styled-content> and 11 IHA<\/jats:styled-content>) the titer was evaluated under mineralocorticoid receptor (MR<\/jats:styled-content>) antagonist treatment. We found that PA<\/jats:styled-content> patients had a significantly higher titer of AT<\/jats:styled-content>1RA<\/jats:styled-content>b compared with controls (median values 33 [IQR<\/jats:styled-content> 15.6] IU\/mL vs 17.5 [IQR<\/jats:styled-content> 10.8] IU<\/jats:styled-content>\/mL, respectively; P\u00a0<\/jats:italic><\u00a00.0001). No significant difference of the AT<\/jats:styled-content>1RA<\/jats:styled-content>b titer was reported among PA<\/jats:styled-content> patients, subdivided according to the subtypes and the concomitant MR<\/jats:styled-content> antagonist therapy. No significant correlation was detected between age, gender, BMI<\/jats:styled-content>, blood pressure values, baseline aldosterone, ARR<\/jats:styled-content>, and the AT<\/jats:styled-content>1RA<\/jats:styled-content>b titer of all patients enrolled. Our data confirm an increased titer of AT<\/jats:styled-content>1RA<\/jats:styled-content>b in both subtypes of PA<\/jats:styled-content>, independently from the concomitant use of MR<\/jats:styled-content> antagonists and clinical\/biochemical characteristics of PA<\/jats:styled-content> patients. The small sample of patients and the relatively short time of treatment could have influenced these results. Moreover, the ELISA<\/jats:styled-content> assay fails to evaluate the bioactivity of AT<\/jats:styled-content>1RA<\/jats:styled-content>b. Further studies should evaluate if the subtype, the clinical\/biochemical recovery of PA<\/jats:styled-content>, or both, influence the pathogenetic role of AT<\/jats:styled-content>1RA<\/jats:styled-content>b. The possible autoimmune pathogenesis and reversal effect with AT<\/jats:styled-content>1R blocker treatment in PA<\/jats:styled-content> patients with AT<\/jats:styled-content>1RA<\/jats:styled-content>b positivity is intriguing and requires further study.<\/jats:p>","DOI":"10.1111\/jch.13351","type":"journal-article","created":{"date-parts":[[2018,7,30]],"date-time":"2018-07-30T03:44:03Z","timestamp":1532922243000},"page":"1313-1318","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Evaluation of angiotensin II<\/scp> type\u20101 receptor antibodies in primary aldosteronism and further considerations about their possible pathogenetic role"],"prefix":"10.1111","volume":"20","author":[{"given":"Chiara","family":"Sabbadin","sequence":"first","affiliation":[{"name":"Department of Medicine, Endocrinology University of Padova Padova Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Filippo","family":"Ceccato","sequence":"additional","affiliation":[{"name":"Department of Medicine, Endocrinology University of Padova Padova Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eugenio","family":"Ragazzi","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical and Pharmacological Sciences University of Padova Padova Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marco","family":"Boscaro","sequence":"additional","affiliation":[{"name":"Department of Medicine, Endocrinology University of Padova Padova Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Corrado","family":"Betterle","sequence":"additional","affiliation":[{"name":"Department of Medicine, Endocrinology University of Padova Padova Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6433-5155","authenticated-orcid":false,"given":"Decio","family":"Armanini","sequence":"additional","affiliation":[{"name":"Department of Medicine, Endocrinology University of Padova Padova 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