MON-767 "Revisiting the Interaction Between Aldosterone and Bone Metabolism: Improvement of Hyperparathyroidism After Treatment for Primary Hyperaldosteronism - A Case Series Report”

Abstract Disclosure: M.N. Ohe: None. W.D. Fernandes: None. O.M. Ammar: None. M.Y. Melo: None. L.S. Fraga: None. M. Lazaretti-Castro: None. S.S. Maeda: None. F.A. Barbosa: None. J.G. Vieira: None. Background: Evidence suggests a bidirectional relationship between parathyroid hormone (PTH) and aldosterone. However, the direct effects of aldosterone on bone metabolism remain poorly understood. Here, we present 4 cases of primary hyperaldosteronism (PA) associated with hyperparathyroidism, and examine the improvement in hyperparathyroid conditions following treatment for PA. Cases report: Case 1: 74 yr woman, hypertension (HTN) since her 40s, post-menopausal osteoporosis and multiple fractures. PTH:149pg/ml (VR 12-65), total calcium (CaT):8.3mg/dL (VR 8.3-10.6), ionized calcium (Cai):1.08mmol/L (VR:1.16-1.32), 25OHD:20.4ng/mL, urinary calcium (CaU):428mg/24hs (VR<250mg), potassium (K):3.4mEq/L (VR:3.5-5.1), aldosterone/renin ratio (A/R):43 (VR<27), plasma renin activity (PRA)<0.04ng/mL/h (VR:0.2-3.3). Diagnosis of PA due to adrenal hyperplasia was made and treatment with spironolactone 75mg/day was initiated. New tests: PTH:42.7pg/ml, CaT:9.4mg/dL, Cai:1.18mmol/L, 25OHD:28.5ng/mL, CaU:100mg/24hs, K:5.1mEq/L, PRA:1.85ng/ml/h. Case 2: 56 yr, male, multiple fractures and nephrolithiasis, HTN, bariatric surgery at 50 yr. PTH:80pg/ml, CaT:9.7mg/dL, Cai:1.3mmol/L, 25OHD:46ng/mL, CaU:135mg/24hs (VR < 300mg), K:2.9mEq/L, aldosterone/renin ratio:112. Diagnosis: PA due to a right adrenal adenoma. Treatement: right adrenalectomy. New exams: PTH:43pg/mL, CaT:9.84mg/dL, Cai:1.32mmol/L, 25OHD:47ng/mL, CaU:87mg/24hs, K:4.4mEq/L, A/R:3. Case 3: 51yr, woman, HTN since her 30s. PTH:81pg/mL, CaT:8.8mg/dL, Cai:1.19mmol/L, 25OHD:30ng/ml, CaU:267mg/24hs (5.3mg/kg). Treatement: hydrochlorothiazide (HCTZ), for idiopathic hypercalciuria. Due to hypokalemia, years after starting HCTZ, screening for PA was performed: A/R ratio (2 tests):28.3 and 29.2. Etiology: adrenal hyperplasia. Treatment: spironolactone was indicated and HCTZ was discontinued. New exams: PTH:36pg/mL, CaT:9.4mg/dL, Cai:1.23mmol/L, 25OHD:47ng/mL, CaU:151mg/24hs. Case 4: 56 yr, woman, HTN at 32y, nephrolithiasis, hypercalciuria, submitted to left inferior parathyroidectomy at 40y due to primary hyperparathyroidism. Exams after parathyroidectomy: PTH:71pg/mL, CaT:9.6mg/dL, Cai:1.35mmol/L, 250HD:42ng/mL, CaU 97mg/24hs, A/R ratio 32. Diagnosis: PA. Treatment: spironolactone 75mg/day. New exams: PTH:55pg/mL, CaT:9.4mg/dL, Cai:1.32mmol/L, 250HD:43ng/mL, CaU:87mg/24hs, A/R 9.5. Conclusion: The reported cases underscore the importance of considering primary aldosteronism as a potential cause of hypercalciuria and isolated PTH elevation. The renin-angiotensin-aldosterone system and the calcium-PTH axis are interconnected. The impact of PA on mineral and bone metabolism should be taken into account, as clinical/surgical treatment of PA can mitigate and/or reverse osteometabolic disorders. Presentation: Monday, July 14, 2025