A Case of Abiraterone-Induced Mineralocorticoid Excess Syndrome Associated with Rhabdomyolysis and Polyuria

Introduction: Abiraterone is an androgen biosynthesis inhibitor used in treatment of metastatic prostate cancer. The goal of therapy is to decrease growth of androgen-sensitive prostate cancer cells. The American Urological Association recommends administering abiraterone in combination with prednisone. When this therapy is conducted without concomitant prednisone, it has been associated with increased mineralocorticoid levels leading to hypokalemia and secondary hypertension. While this is a well-known sequela of treatment, a less observed occurrence of rhabdomyolysis and polyuria can be seen through downstream effects of chronic hypokalemia. Case Description: We present an 85-year-old male with history of metastatic prostate cancer who experienced mineralocorticoid excess syndrome. This patient was initially started on abiraterone and prednisone. The subsequent testosterone and prostate-specific antigen levels were appropriately low. After being lost to follow-up, this patient had continued taking abiraterone without prednisone for 9-months. The patient then presented with weakness resulting in a fall. The creatinine kinase level was greater than detectable on assay. Given preserved renal function, balanced crystalloids were used to prevent heme-pigment nephropathy. While rhabdomyolysis is often associated with hyperkalemia, potassium levels were found to be chronically decreased prior to admission and remained 2.5-3 mmol/L despite ample repletion. In addition, urine output (7.5-10L/day) exceeded that of intake volume. After resuming prednisone and starting amiloride, his hyperkalemia resolved first, followed by gradual resolution of rhabdomyolysis and polyuria. Discussion: We believe that this case report highlights the rarer effects of chronic hypokalemia. First, rhabdomyolysis can be observed due to hypokalemia-induced dysregulation of skeletal muscle blood flow. Second, there has been historical reports of hypokalemia-associated tubular concentrating defects through disruption of AQP2 production. Despite treatment, both rhabdomyolysis and polyuria continued until successful normalization of serum potassium suggesting that the hypokalemia was the primary driver of our patient's presentation.