Abstract: PUB077
Status Epilepticus With an AKI
Session Information
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Author
- Malik, Ayesha M., LSU Health Shreveport, Shreveport, Louisiana, United States
Introduction
Acute uric acid nephropathy is characterized by oliguric renal failure due to overproduction of uric acid and it’s deposition in renal tubules. This typically occurs in cases of leukemias and lymphomas or following chemotherapy due to tumor lysis. A few cases have reported uric acid crystals in the urine of patients with status epilepticus (1,2,5). Seizures can cause direct nucleotide breakdown, producing adenosine which is converted to uric acid in the liver. Serum nucleotidase activity can be elevated for several hours after seizures, increased systemic breakdown of adenosine triphosphate, generating urate (1). Seizures cause dehydration and hyperthermia resulting in increased water reabsorption. This increases concentration of uric acid in urine, precipitates in renal tubules. it can cause direct damage to kidneys by activating pro-inflammatory mediators inducing renal vasoconstriction (3).
Case Description
64 year old woman with history of glioblastoma multiforme status post multiple craniotomies for resection, admitted with status epilepticus. She required a midazolam drip and was intubated for airway protection. She subsequently became bradycardic, hypothermic and anuric and remained so for the next 3 days despite 5L of crystalloids. Her creatinine increased from 0.5 to 1.8mg/dl and she developed anasarca. Laboratory studies were significant for BUN 28, C02 17mmol/L, CPK 18U/L and BNP 554 pg/ml. Her renal ultrasound was normal. Initial urine analysis showed a pH of 5 with bland sediment. A second bedside urine analysis performed a few days later revealed abundant uric acid crystals, but no muddy brown casts or RTECs. In the absence of any other etiology for the AKI, a diagnosis of acute uric acid nephropathy was made and she was started on a bicarbonate drip along with furosemide to keep urine pH 6.5-7. Her urine output consequently increased and creatinine normalized.
Discussion
Urinalysis with microscopic examination of urine sediment is an important clinical tool for diagnosing AKI. Varghese et al showed that 20-25% cases which yielded no diagnosis on first urine microscopy, showed casts representing acute tubular injury on a second or third urine microscopy done 2-3 or 4-6 days later.(4) In our case, uric acid crystals were identified on a second urine microscopy while the first one was clear. Serial exams may be helpful in uncovering the cause of AKI which a single inspection may miss.