Mifepristone-Induced Hypokalemia Causing Rhabdomyolysis and Severe Acute Kidney Injury: A Case Report
Abstract
Mifepristone is a glucocorticoid receptor (GR) blocker approved for improving glucose control in patients with endogenous Cushing’s Syndrome (CS) in whom surgical cure is contraindicated or has failed. Due to GR blockade, levels of ACTH and cortisol become markedly higher. When cortisol levels are sufficiently high, the enzyme conferring aldosterone specificity to the aldosterone-sensitive distal nephron, 11β-hydroxysteroid dehydrogenase type 2, that converts active cortisol to inactive cortisone may be overwhelmed. The result may be enhanced renal potassium excretion and hypokalemia. We report a case of a patient with suspected CS given mifepristone to improve glucose control. The patient subsequently presented with rhabdomyolysis and severe acute kidney injury (AKI) requiring emergency dialysis. Kidney biopsy confirmed myoglobinuria as the cause of the AKI. Despite ongoing cell breakdown, severely reduced GFR, dialysis against a high potassium bath, and daily potassium replacement, the serum potassium took days to normalize. We postulate that mifepristone-induced severe potassium deficiency with hypokalemia was the trigger for rhabdomyolysis and AKI in this patient. This case highlights the vigilance for hypokalemia required when mifepristone is given for improving glucose control.
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Evidence Hub reads this as a case report, done in people. Its evidence level is 5 of 5 (Very low · case / narrative / animal / in vitro / in silico). Case reports, narrative reviews, and animal, cell or computer-model studies give the weakest evidence for human health.
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