Open AccessEvaluation of angiotensin II type‐1 receptor antibodies in primary aldosteronism and further considerations about their possible pathogenetic role
Author(s) -
Sabbadin Chiara,
Ceccato Filippo,
Ragazzi Eugenio,
Boscaro Marco,
Betterle Corrado,
Armanini Decio
Publication year - 2018
Publication title -
the journal of clinical hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 67
eISSN - 1751-7176
pISSN - 1524-6175
DOI - 10.1111/jch.13351
Subject(s) - medicine , primary aldosteronism , titer , concomitant , aldosterone , hyperaldosteronism , endocrinology , autoantibody , angiotensin ii , antagonist , receptor , gastroenterology , pathogenesis , renin–angiotensin system , antibody , blood pressure , immunology
Angiotensin II type‐1 receptor autoantibodies ( AT 1 RA b) have been involved in the genesis of primary aldosteronism ( PA ), both in aldosterone‐producing adenoma ( APA ) and in idiopathic hyperaldosteronism ( IHA ). In this study, we evaluated the titer of AT 1 RA b in 44 PA patients (15 with APA and 29 with IHA ) compared with 18 normotensive healthy controls who were matched for gender and age. In 17 PA patients (6 APA and 11 IHA ) the titer was evaluated under mineralocorticoid receptor ( MR ) antagonist treatment. We found that PA patients had a significantly higher titer of AT 1 RA b compared with controls (median values 33 [ IQR 15.6] IU/mL vs 17.5 [ IQR 10.8] IU /mL, respectively; P < 0.0001). No significant difference of the AT 1 RA b titer was reported among PA patients, subdivided according to the subtypes and the concomitant MR antagonist therapy. No significant correlation was detected between age, gender, BMI , blood pressure values, baseline aldosterone, ARR , and the AT 1 RA b titer of all patients enrolled. Our data confirm an increased titer of AT 1 RA b in both subtypes of PA , independently from the concomitant use of MR antagonists and clinical/biochemical characteristics of PA patients. The small sample of patients and the relatively short time of treatment could have influenced these results. Moreover, the ELISA assay fails to evaluate the bioactivity of AT 1 RA b. Further studies should evaluate if the subtype, the clinical/biochemical recovery of PA , or both, influence the pathogenetic role of AT 1 RA b. The possible autoimmune pathogenesis and reversal effect with AT 1R blocker treatment in PA patients with AT 1 RA b positivity is intriguing and requires further study.