Ogilvie Syndrome and Abiraterone: Untangling Two Uncommon Causes of Refractory Hypokalemia

Introduction: This case highlights the clinical approach and challenges in diagnosing and treating hypokalemia when multiple rare etiologies are present. Case Description: A 73 year old male with past medical history of metastatic prostate cancer, complicated by lower extremity paralysis and chronic urinary retention, chronic adrenal insufficiency, hypertension, and Ogilvie’s syndrome, who presented to our hospital with severe, refractory hypokalemia. He had recently been admitted for sepsis and persistent hypokalemia, during which time his urine potassium/creatinine (K/Cr) ratio was 3.5, and fractional excretion of potassium 10.42 (normal range), which suggested renal wasting for the degree of hypokalemia. Additionally, magnesium was in normal range, aldosterone level was low, ACTH level was elevated with low serum cortisol. He was started on medication regimen of Amiloride, Eplerenone, and prednisone. Patient was managed on outpatient potassium tablets but was later re-admitted after outpatient labs showed potassium level of 2.3. Urine studies showed urine K/Cr ratio 0.97, stool potassium 150, and stool osmolality 564, reflective of ongoing stool potassium losses but resolution of renal potassium losses while on Amiloride and Eplerenone. Based on imaging studies significant for colonic distension, he was treated for Ogilvie’s syndrome with eventual improvement in potassium levels and was discharged. Discussion: Abiraterone induced renal potassium wasting is a well-known cause of refractory hypokalemia and affects up to 30% of patients taking the medication. This medication inhibits 17 alpha-hydroxylase responsible for producing androgens. By way of reducing negative feedback on ACTH, this leads to excess mineralocorticoid production from adrenal glands. In this patient, treatment with Eplerenone and Amiloride suppressed mineralocorticoid production. An even more rare cause of hypokalemia is colonic pseudo-obstruction (or Ogilvie’s syndrome) which is associated with marked overexpression of the BK channel in both surface and crypt colonocytes as well as the renal collecting duct. This results in increased sensitivity to normal serum aldosterone levels and persistent, predominantly colonic, potassium wasting. This explains this patient’s improvement on aldosterone antagonists, as it worked to suppress expression of BK channels, as well as treatment of pseudo-obstruction.