Elevation of Angiotensin-II Type-1-Receptor Autoantibodies Titer in Primary Aldosteronism as a Result of Aldosterone-Producing Adenoma

Primary Aldosteronism Hyperaldosteronism Adrenal adenoma
DOI: 10.1161/hypertensionaha.112.202945 Publication Date: 2012-12-18T05:43:21Z
ABSTRACT
The mechanisms of excess aldosterone secretion in primary aldosteronism (PA) remain poorly understood, although a role for circulating factors has been hypothesized decades. Agonistic autoantibodies against type-1 angiotensin-II receptor (AT1AA) are detectable malignant hypertension and preeclampsia might play PA. Moreover, if they were elevated aldosterone-producing adenoma (APA) not idiopathic hyperaldosteronism (IHA), be useful discriminating between these conditions. To test hypotheses, we measured the titer AT1AA serum 46 patients with PA (26 APA, 20 IHA), 62 (PH), 13 preeclamptic women, 45 healthy normotensive blood donors.We found that was higher ( P <0.05) both PH (2.65±1.55 1.86±0.63, respectively) than subjects (1.00±0.20). In it 2-fold IHA (3.43±1.20 versus 1.64±1.39, respectively, <0.001), despite similar pressure values. Of note, allowed effective discrimination APA from either or IHA, as shown by Receiver Operator Characteristics curve analysis. after captopril challenge, plasma concentration fell more AT1AA-positive AT1AA-negative (–32.4% [21.1–42.9] 0.0% [0.0–22.6], =0.015), suggesting an agonistic autoantibodies. Thus, can differentiating thus selecting to submitted adrenal vein sampling.
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