title: Elevation of angiotensin-II type-1-receptor autoantibodies titer in primary aldosteronism as a result of aldosterone-producing adenoma.
abstract: The mechanisms of excess aldosterone secretion in primary aldosteronism (PA) remain poorly understood, although a role for circulating factors has been hypothesized for decades. Agonistic autoantibodies against type-1 angiotensin-II receptor (AT1AA) are detectable in malignant hypertension and preeclampsia and might play a role in PA. Moreover, if they were elevated in aldosterone-producing adenoma (APA) and not in idiopathic hyperaldosteronism (IHA), they might be useful for discriminating between these conditions. To test these hypotheses, we measured the titer of AT1AA in serum of 46 patients with PA (26 with APA, 20 with IHA), 62 with primary hypertension (PH), 13 preeclamptic women, and 45 healthy normotensive blood donors.We found that the AT1AA titer was higher (P<0.05) in both PA and PH patients (2.65 ± 1.55 and 1.86 ± 0.63, respectively) than in normotensive subjects (1.00 ± 0.20). In APA, it was 2-fold higher than in IHA patients (3.43 ± 1.20 versus 1.64 ± 1.39, respectively, P<0.001), despite similar blood pressure values. Of note, it allowed effective discrimination of APA from either PH or IHA, as shown by Receiver Operator Characteristics curve analysis. Moreover, after captopril challenge, plasma aldosterone concentration fell more in AT1AA-positive than in AT1AA-negative PA patients (-32.4% [21.1-42.9] versus 0.0% [0.0-22.6], P=0.015), suggesting an agonistic role for these autoantibodies. Thus, a higher serum AT1AA titer in patients with APA than in IHA and PH patients can be useful in differentiating APA patients from either PH or IHA, and thus in selecting PA patients to be submitted to adrenal vein sampling.
authors.affiliation: Department of Medicine—DIMED, Internal Medicine 4, Padua University—School of Medicine, Padova, Italy.
authors.forename: Giacomo
authors.initials: G
authors.lastname: Rossitto
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Regolisti
authors.forename: Ermanno
authors.initials: E
authors.lastname: Rossi
authors.forename: Aurelio
authors.initials: A
authors.lastname: Negro
authors.forename: Davide
authors.initials: D
authors.lastname: Nicoli
authors.forename: Bruno
authors.initials: B
authors.lastname: Casali
authors.forename: Antonio
authors.initials: A
authors.lastname: Toniato
authors.forename: Brasilina
authors.initials: B
authors.lastname: Caroccia
authors.forename: Teresa Maria
authors.initials: TM
authors.lastname: Seccia
authors.forename: Thomas
authors.initials: T
authors.lastname: Walther
authors.forename: Gian Paolo
authors.initials: GP
authors.lastname: Rossi
mesh_terms: D000236:Adenoma / Q000175:diagnosis / Q000276:immunology / Q000378:metabolism*; D000306:Adrenal Cortex Neoplasms / Q000175:diagnosis / Q000276:immunology / Q000378:metabolism*; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood / Q000378:metabolism*; D001323:Autoantibodies / Q000097:blood*; D015551:Autoimmunity / Q000276:immunology; D003937:Diagnosis, Differential; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000097:blood / Q000175:diagnosis / Q000276:immunology*; D006973:Hypertension / Q000097:blood / Q000276:immunology; D008875:Middle Aged; D011225:Pre-Eclampsia / Q000097:blood / Q000276:immunology; D011247:Pregnancy; D044140:Receptor, Angiotensin, Type 1 / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D044140:Receptor, Angiotensin, Type 1; D000450:Aldosterone