SUN-365 Characteristics of Primary Aldosteronism without Suppression of Plasma Renin Activity

Abstract

Abstract Introduction: Primary aldosteronism (PA) is a common cause of secondary hypertension. It is characterized by excess production of aldosterone from the adrenal glands resulting in suppressed plasma renin activity (PRA) by a negative feedback regulation. Thus, if a patient with hypertension had an unsuppressed PRA, the possibility of PA might be excluded. However, we have observed some PA patients with unsuppressed PRA in our hospital. Here, we report clinical characters of PA patients with unsuppressed PRA. Methods: We searched for PA patients with unsuppressed PRA (Escaped PRA group) from 969 patients who underwent segmental adrenal venous sampling (S-ATS) in our hospital between April 2009 and March 2018. Escaped PRA group were those with PRA level of >1.0 ng/mL/hr in any two or more blood samples obtained in resting position, and had aldosterone producing adenomas (APAs) in which CYP11B2 expression was confirmed histopathologically. We also enrolled patients with APAs with suppressed PRA as a control group (34 females, 35 females ). All patients in the control group had PRA level of < 1.0 ng/mL/hr in any two or more blood samples obtained in resting position and had macroadenomas in which CYP11B2 expression was confirmed. We compared clinical characteristics between Escaped PRA group and Control group. Results: We found that 7 cases (3 males, 4 females) were in the Escaped PRA group (PRA; 2.3±0.8 ng/mL/hr). One of them showed a gap between PRA and Active Renin Concentration (ARC). Compared to the control group (PRA; 0.3±0.2 ng/mL/hr), the escaped PRA group had no significant difference in body mass Index, blood pressure, urinary aldosterone, and serum potassium. The escaped PRA group tended to be younger compared to control group (53.0±4.4 years-old vs 47.4±10.8 years-old, P = 0.12) and have decreased eGFR Escaped (74.4±20.0 mL/min/1.73 m2 vs 86.3±19.3 mL/min/1.73 m2, P = 0.088). Only serum cortisol level after 1 mg dexamethasone suppression test showed a significant difference (Escaped PRA group; 1.9±0.5 mg/dL, Control group 1.4±3.0 mg/dL, P = 0.011). Conclusion: Excess cortisol has been reported to increase PRA through increasing renin substrate and suppressing ACTH-dependent aldosterone secretion. We should not exclude the possibility of PA in patients without suppressed plasma renin activity, especially who had a cortisol excess.