Abstract P274: Double Hit! A Unique Case of Resistant Hypertension

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2017-09, Vol.70 (suppl_1)
• Main Authors: DeCarlo, Kristen, Agrawal, Nidhi
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.70.suppl_1.p274

Abstract only Case Description: A 52 year-old woman with obesity, HLD, diet-controlled diabetes was referred for resistant hypertension. Her blood pressure (BP) was uncontrolled (systolic 145-200 mmHg, diastolic 95-135 mmHg) on 5 medications. Physical exam revealed a systolic ejection murmur at the base. An ECHO showed normal systolic function and moderate LVH. Plasma aldosterone was 20.7 ng/dL (normal 3-15 g/dL), plasma renin was 0.50 ng/mL/h (normal 0.65-5.0 ng/mL/h), and aldosterone:renin ratio was 41.4 [ng/dL]/[ng/mL/h], meeting criteria for Primary Aldosteronism (PA). Saline infusion test was confirmatory for PA. CT scan of the adrenals did not reveal an adenoma. Subsequent Adrenal Venous Sampling confirmed bilateral Idiopathic Adrenal Hyperplasia (IAH; right and left adrenal vein selectivity index of 42.6, 9.2 respectively; lateralization index was 1.3). She was normokalemic (3.7-4.4 mEq/L), total calcium (Ca) was 11.2 mg/dL (normal Ca 8.0-10.4), and creatinine was 1.4 mg/dL (GFR 47 mL/min/1.73m 2 ). Intact parathyroid hormone (iPTH) was 131.2 pg/mL, phosphorus was 2.4 mg/dL, and 25-hydroxyvitamin D was 30.8 ng/mL, suggesting primary hyperparathyroidism (PPTH). Neck ultrasound was concerning for PTH adenoma and sestamibi scan localized a left adenoma. DXA scan and renal ultrasound were normal. IAH was treated medically with spironolactone. Her BP remained elevated (systolic 138-172 mmHg, diastolic 92-100 mmHg). She underwent parathyroidectomy and histology confirmed an adenoma. Post-operative iPTH and Ca normalized (49.5 pg/mL, 9.7 mg/dL respectively). Postoperative BP measurements improved (systolic 123-138 mmHg, diastolic 75-86 mmHg). Discussion: Evidence shows that a hyperfunctioning parathyroid gland may contribute to maintaining hyperaldosteronism in PA. This is based on in-vitro studies showing PTH increased aldosterone secretion from adrenocortical cells in a concentration dependent manner. Gene expression and immunohistochemistry studies show PTH receptors in aldosterone-producing adenomas and MR receptors in parathyroid cells, suggesting a bi-directional relationship. The significance of this case is in the potential for further understanding of the pathophysiology of common causes of secondary hypertension.