Abstract: TH-PO0213
High Stakes Under Low Androgens: Amiloride Conquers Abiraterone-Driven Resistant Hypertension
Session Information
- Onconephrology: Anticancer Therapies, PTLD, Paraneoplastic Diseases, and More
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1700 Onconephrology
Authors
- Smith, Zachary, University of Cincinnati, Cincinnati, Ohio, United States
- Gaur, Mragank, University of Cincinnati, Cincinnati, Ohio, United States
- Gudsoorkar, Prakash Shashikant, University of Cincinnati, Cincinnati, Ohio, United States
Introduction
Abiraterone (ABI) - FDA 2018, high-risk metastatic castration-sensitive prostate cancer (PC) blocks CYP17A1, triggers mineralocorticoid excess, and causes hypertension (HTN) in up to 22 % of patients (grade 3–4 HTN in 10 %). Resistant-HTN (rHTN) rates are unknown; mineralocorticoid-receptor antagonists (MRA) are avoided for possible androgen-receptor (AR) activation.
Case Description
A 70-year-old man with metastatic PC, diabetes (metformin), no prior HTN, began ABI + prednisone. Baseline BP was 128/78 mm Hg; serum creatinine (Scr) was 1.0 mg/dL, eGFR was 79 mL/min/1.73 sqm, and urine protein was undetectable. At week 12, the patient’s BP reached 150/90 mmHg, so the PCP began amlodipine 10 mg once daily. By week 20, it had risen to 180/100 mmHg; the onconephrology team therefore added valsartan 320 mg daily. BP remained persistently elevated at 165/102 mmHg at week 28, leading to the introduction of chlorthalidone 25 mg daily. When the BP remained at 155/95 mmHg at week 32, rHTN was diagnosed, and amiloride 5 mg was started daily. A secondary-hypertension work-up (aldosterone-renin ratio, plasma/urine metanephrine, renal-artery doppler) was unremarkable. With readings still 150/92 mmHg at week 36, the amiloride dose was increased to 5 mg twice daily, achieving control at 125/83 mmHg by week 40.
Discussion
ABI-induced hypertension arises when CYP17A1 blockade lowers cortisol, provoking an ACTH surge that with the mineralocorticoid precursors 11-deoxycorticosterone and corticosterone; their receptor activation causes sodium retention, hypokalaemia, and marked BP elevation even in patients without prior cardiovascular disease. This patient's hypertension persisted despite amlodipine, valsartan, and chlorthalidone but fell to 125/83 mmHg once amiloride, a potassium-sparing blocker of distal sodium reabsorption that does not engage the AR, replaced MRA that might blunt ABI's anticancer activity. ACEi remain useful adjuncts, yet amiloride offers an androgen-neutral strategy for controlling rHTN during ABI therapy and warrants prospective study.