Renal Potassium Wasting from Abiraterone-Induced Mineralocorticoid Excess Syndrome

Introduction: Abiraterone, a CYP17A1 inhibitor used to treat metastatic prostate cancer, suppresses cortisol and androgen synthesis while increasing mineralocorticoid precursors such as deoxycorticosterone, leading to features of mineralocorticoid excess like hypertension and renal potassium wasting. Glucocorticoids are co-administered to suppress ACTH and mitigate these effects. We present a case of severe, persistent hypokalemia due to inadequate steroid replacement in a patient on chronic abiraterone therapy. Case Description: A 78-year-old male with metastatic prostate cancer on androgen deprivation therapy since 2020, was admitted for severe hypokalemia. His medications included abiraterone and prednisone 5 mg daily. His BP was 160/75, and physical examination was unremarkable. Labs showed potassium 2.2 mEq/L, magnesium 1.6 mg/dL, phosphorus 1.4 mg/dL, and metabolic alkalosis (pH 7.46, HCO3- 30 mEq/L). The hypokalemia was initially attributed to refeeding syndrome, but it persisted despite aggressive potassium repletion and correction of other abnormalities. Historical labs revealed recurrent hypokalemia (nadir 3.0 mEq/L). Hormonal evaluation showed suppressed AM cortisol (2.6 mcg/dL), with normal ACTH (16 pg/mL), renin (0.176 ng/mL/hr), and aldosterone (9.7 ng/dL). Urine potassium was 36.9 mEq/L with concurrent serum potassium of 3.6 mEq/L, yielding a TTKG of 6, consistent with renal potassium wasting. Increasing the prednisone dose to 5 mg twice daily led to normalization of serum potassium without further need for potassium supplementation. Discussion: This case highlights the importance of recognizing abiraterone-induced mineralocorticoid excess as a cause of persistent hypokalemia. In our patient, although ACTH was not elevated as would be expected with low serum cortisol, its suppression was likely due to chronic steroid therapy. The initial prednisone dose was inadequate, and a higher dose was needed to fully suppress ACTH and downstream mineralocorticoid production. Clinicians should maintain a high index of suspicion for this syndrome and routinely evaluate the adequacy of steroid co-administration in patients receiving abiraterone.