Mefenamic Acid Poisoning Revisited: Central Nervous System Toxicity and Acute Kidney Injury

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a common cause of acute poisoning and often perceived as relatively benign in overdose. Mefenamic acid is unique among NSAIDs in that it is not available over-the-counter in many countries and may have a higher risk of central nervous system toxicity than other NSAIDs. Despite previous reports of seizures and renal dysfunction due to mefenamic acid poisoning, detailed information on the toxicity and the blood concentrations in recent case reports remains limited. A 22-year-old woman presented with two episodes of generalized tonic-clonic seizures three hours after intentional ingestion of multiple analgesics, including 2.5 g (60 mg/kg) of mefenamic acid. On admission, she was agitated but neurologically intact. Initial laboratory findings showed normal renal function. She was admitted for observation. On day 3, she developed acute kidney injury (AKI) with a peak creatinine of 4.21 mg/dL. Her renal dysfunction gradually resolved without dialysis. Drug concentration analysis showed a serum mefenamic acid level of 42.2 µg/mL at admission (toxic threshold: 25 µg/mL). Based on clinical findings and drug concentrations, seizures and AKI were attributed to mefenamic acid poisoning. Mefenamic acid poisoning can result in neurological and renal complications even at modest doses. Given its common use in dysmenorrhea and overlapping demographic with at-risk populations for overdose, clinicians should maintain a high index of suspicion and monitor closely when mefenamic acid ingestion is suspected. Further reports are needed to clarify relationships between serum concentrations, ingested dose, and clinical severity.