Abstract

Acute hyperuricemia most commonly occurs in patients who experience tumor lysis syndrome. Hyperuricemia along with other electrolyte abnormalities like hyperkalemia, hypocalcemia, and hyperphosphatemia leads to acute kidney injury (AKI) due to acute uric acid nephropathy which is associated with significant morbidity. High risk patients are thus closely monitored for signs of these laboratory abnormalities. Extreme exercise, rhabdomyolysis, and seizures are rare causes of acute hyperuricemia. Serum uric acid level is not routinely monitored as a part of postictal labs. We report an unusual case of AKI in a young male with recurrent seizures and no associated rhabdomyolysis who was found to have acute uric acid nephropathy. Timely administration of Rasburicase prevented the need for dialysis in this patient and led to complete renal recovery. This case illustrates the importance of doing a urine microscopy and checking uric acid level in patients with recurrent seizures who develop unexplainable AKI, as timely management helps improve outcome. We also briefly review the pathophysiology of seizure related hyperuricemia and acute uric acid nephropathy.

Highlights

  • Uric acid is the final end product of purine metabolism

  • Acute hyperuricemia is caused by the increase of purine metabolism, which is the result of the increased cellular turnover or the aggressive cancer chemotherapy regimens which cause cell lysis and release of purine metabolites [1]

  • We report a patient who developed acute kidney injury (AKI) due to acute uric acid nephropathy following recurrent seizures

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Summary

Introduction

Uric acid is the final end product of purine metabolism. Acute hyperuricemia is caused by the increase of purine metabolism, which is the result of the increased cellular turnover or the aggressive cancer chemotherapy regimens which cause cell lysis and release of purine metabolites [1]. Acute uric acid nephropathy is readily recognized when acute kidney injury (AKI) develops in cancer patients either due to spontaneous tumor lysis or following chemotherapy. Seizures seldom cause acute hyperuricemia and acute uric acid nephropathy and its diagnosis may be missed or delayed in this uncommon presentation. With timely recognition and management, the pathologic features of acute uric acid nephropathy are reversible. We report a patient who developed AKI due to acute uric acid nephropathy following recurrent seizures. Therapy with Rasburicase prevented the need for renal replacement therapy in our patient and resulted in complete renal recovery

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