Abiraterone-Induced Hypokalemia and Hypophosphatemia: A Case Report

Abiraterone acetate is a commonly used androgen biosynthesis inhibitor in the management of advanced prostate cancer and is associated with mineralocorticoid excess due to CYP17 inhibition. This can result in electrolyte abnormalities, most notably hypokalemia, which may be severe and refractory to standard replacement therapy. We present the case of an 82-year-old male with metastatic prostate cancer on abiraterone therapy who was admitted with altered mental status, hyponatremia, and acute kidney injury in the setting of poor oral intake. Despite appropriate volume resuscitation and electrolyte replacement, the patient developed persistent hypokalemia and hypophosphatemia with evidence of renal potassium wasting. Given the clinical context, abiraterone-induced mineralocorticoid excess was suspected. As discontinuation of abiraterone was not feasible, treatment with the mineralocorticoid receptor antagonist spironolactone was initiated, resulting in sustained correction of electrolyte abnormalities. This case highlights the need to consider abiraterone-induced mineralocorticoid excess in patients with refractory hypokalemia, particularly when renal potassium wasting persists after correction of volume status and kidney function. Early recognition may prevent prolonged hospitalization, treatment delays, and serious complications. When abiraterone must be continued, mineralocorticoid receptor antagonists can provide targeted therapy while preserving cancer treatment. This case also emphasizes the importance of routine electrolyte monitoring in patients receiving abiraterone, even when they are prescribed concurrent prednisone.