Abstract: SA-PO0089
Wrestling with Kidney Injury: A Rare Case of Levetiracetam-Induced Acute Interstitial Nephritis
Session Information
- AKI: Clinical Diagnostics and Biomarkers
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Vayder, Luke T, Des Moines University, West Des Moines, Iowa, United States
- Malik, Abu-Bakr Azam, MercyOne Internal Medicine Residency Program, Des Moines, Iowa, United States
Introduction
Acute Kidney Injury (AKI) is the sudden decrease in renal function defined as: an increase in serum creatinine ≥ 0.3 mg/dl within 48 hours, an increase in serum creatinine to ≥ 1.5 times the known or presumed baseline within the prior 7 days, or a urine volume of < 0.5 ml/kg/hour for 6 hours. Acute Interstitial Nephritis (AIN), an often overlooked cause of AKI, should be suspected in patients with eosinophilia, urine eosinophils, and urine WBC casts. Several drug classes have been reported to cause AIN such as: beta-lactams, NSAIDs, PPIs, and anticonvulsants.
Case Description
A 24-year-old male wrestler presented to the emergency room after a ground-level fall associated with a seizure. His past medical history was notable for seizures for which he was not receiving anti-epileptic therapy. A head CT showed a small left-sided subarachnoid hemorrhage without midline shift and a subdural hemorrhage. Due to his acute mental status and compromised ventilation, he was intubated and admitted to the ICU. Neurology was consulted, and he was started on levetiracetam for seizure prophylaxis. 48 hours later, he developed AKI with a concomitant metabolic acidosis. Eosinophils were noted in his urine. Levetiracetam was discontinued, as AIN was suspected, and alternative therapy with lacosamide was started. His kidney function improved, and he was discharged in stable condition.
Discussion
Levetiracetam is a widely used and well tolerated anti-epileptic used in seizure prophylaxis. Although rare, AIN has been reported in a handful of cases as an adverse reaction to levetiracetam. Our patient developed AKI shortly after administration of levetiracetam, raising suspicion for a drug-induced immune-mediated reaction. AIN is typically a hypersensitivity response involving T-cell mediated inflammation of the renal interstitium which may present with nonspecific findings making diagnosis challenging. Prompt discontinuation of the offending agent and daily monitoring of renal function is the cornerstone of therapy and led to a positive outcome in our case without the need for corticosteroids. This case highlights the importance of maintaining a broad differential when evaluating new AKI. Clinicians should be aware of rare, but serious, adverse reactions associated with commonly used drugs and consider AIN in the appropriate clinical context.