MON-298 Adrenal artery embolization for bilateral primary aldosteronism

Abstract Disclosure: Z. Yuhao: None. H. Minzhi: None. L. Zhenjie: None. J. Yongli: None. Z. Tianyue: None. X. Xiaohong: None. S. Xiaoxiao: None. A 57-year-old male with a 19-year history of hypertension visited the clinic four years ago due to refractory hypertension with hypokalemia. His blood pressure (BP) was 184/113 mmHg, and his K+ was 1.9 mmol/L. After symptomatic treatment, he was referred to our center. Upon re-evaluation, his aldosterone was 2220 pg/mL, renin was 12.2 uIU/mL, and the aldosterone-to-renin ratio (ARR) was 182 (pg/mL)/(uIU/mL). His creatinine reached 94.2 μmol/L. A CT scan revealed bilateral adrenal adenomas (right: 23×21 mm, left: 20×17 mm), and renal artery stenosis was ruled out. Both the captopril and saline tests failed to suppress aldosterone. Adrenal venous sampling (AVS) suggested bilateral aldosterone secretion (lateralization index = 1.3, right/left). The patient was treated with spironolactone 40 mg BID→60 mg TID, nifedipine 30 mg BID, irbesartan 150 mg QD, and potassium chloride 1 g TID→2 g TID. Despite this regimen, his home blood pressure monitoring (HBPM) remained at 160/100 mmHg, with aldosterone at 2280 pg/mL, renin at 83.6 uIU/mL, and ARR at 27.27 (pg/mL)/(uIU/mL). In this period, he developed gynecomastia, erectile dysfunction, hypertensive renal damage (creatinine 120.8 μmol/L, UACR 38.82 mg/g.cr), and ventricular hypertrophy (IVS 1.71 cm). After multidisciplinary discussion, the patient underwent right adrenal artery embolization in July 2023. Postoperatively, his aldosterone decreased to 813 pg/mL, renin increased to 288.5 uIU/mL. His HBPM improved to 145/85 mmHg with reduced doses of spironolactone. However, six months later, his HBPM increased again to 160/100 mmHg, and medications were adjusted to spironolactone 40 mg BID, finerenone 20 mg QD, nifedipine 30 mg BID, irbesartan 150 mg QD, and potassium chloride 1 g BID. His biochemical results showed aldosterone at a2260 pg/mL, renin at 75.6 uIU/mL, ARR at 29.89 (pg/mL)/(uIU/mL), and the renal impairment (creatinine 119.2 μmol/L, UACR 541.25 mg/g.cr). A Ga-68 Pentixafor PET-CT revealed high CXCR4 expression in the left adrenal gland (23×21 mm, SUVmax 35.74) and a postoperative nodule on the right (19×16 mm, SUVmax 9.72). Given the increasing difficulty of medical treatment, further operation was considered. The patient refused surgery and opted for left adrenal artery embolization again.The second procedure was performed in December 2024. After this, his aldosterone was 402 pg/mL, renin was 15.8 uIU/mL, ARR was 25.4 (pg/mL)/(uIU/mL), K+was 3.96 mmol/L, without no signs of corticosteroid insufficiency. His medication regimen included spironolactone 20 mg BID, finerenone 20 mg QD, nifedipine 30 mg BID, irbesartan 150 mg QD, and KCl 1 g BID, maintaining HBPM below 140/80 mmHg. Conclusion: For refractory bilateral primary aldosteronism, bilateral adrenal artery embolization lowers aldosterone levels and reduces antihypertensive medications as a palliative therapy without causing corticosteroid insufficiency. Presentation: Monday, July 14, 2025