From Antifreeze to AKI: A Crystal-Clear Diagnosis

Introduction: Ethylene glycol (EG) poisoning can present with nonspecific symptoms such as altered mental status (AMS) and severe metabolic acidosis. Prompt diagnosis is vital to prevent renal failure and death. We describe a case of EG ingestion causing calcium oxalate nephropathy and reversible anuric AKI. Case Description: A 64-year-old male with hypertension and remote DVT presented as a stroke alert for AMS and weakness. Per his wife, he was well the night prior. In the ED, he was hypertensive (195/110), tachypneic, and hypothermic. Labs showed pH 7.04, HCO3 5, AG 27, serum osmolality 338 (calculated 298; gap 40). Acetaminophen, salicylate, and ethanol levels were negative. Urine tox was positive for benzodiazepines. Urine microscopy revealed numerous birefringent envelope- and cigar-shaped calcium oxalate crystals (Image 1). EG level, drawn before treatment, was 25 mg/dL. He later admitted to antifreeze ingestion in a suicide attempt. Fomepizole was given and intermittent hemodialysis (iHD) initiated on hospital days 1 and 2 for acidosis and rising creatinine. Though initially anuric, urine output returned and creatinine peaked at 7.75 mg/dL before improving. Psychiatry diagnosed major depressive disorder, and he was discharged with nephrology and psychiatry follow-up. Discussion: EG metabolites cause severe high anion gap metabolic acidosis and renal injury via calcium oxalate crystal deposition. Though the EG level was 25 mg/dL, its short half-life and delayed sampling limit diagnostic reliability. This highlights the importance of early empiric treatment based on clinical suspicion, osm gap, and crystalluria. A low or delayed EG level does not exclude toxicity. Anion/osmolar gaps and urine microscopy remain crucial. With timely therapy and dialysis, even anuric AKI can be reversible.