Oluwaseun Oluwo, Anita Vincent-Johnson and Kambiz Kalantari
A young man with a history of pseudo-seizures was admitted after an episode of severe agitation and rigorous physical activity. The patient was febrile on admission with notable leukocytosis and lactic acidosis but a negative infectious workup. During the hospitalization, the patient developed severe Acute Kidney Injury (AKI) despite fluid hydration. Creatinine Phosphoryl Kinase (CPK) was minimally elevated at 693 U/l. Urine
microscopy was significant for many uric acid crystals. Subsequent lab studies revealed an elevated uric acid level of 13.4 mg/dl with fractional excretion of urate (Fe-Urate) of 13%. The patient was treated with rasburicase and allopurinol with the improvement of AKI that paralleled the improvement in hyperuricemia. AKI was likely due to acute urate nephropathy from a pseudo-seizure. AKI following an icteric activity or rigorous physical activity can occur via a mechanism that is independent of rhabdomyolysis. Acute Urate Nephropathy should be considered in cases with no significant elevations of CPK, with prompt initiation of rasburicase and potentially rapid resolution of AKI.
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