Case Study: Ethylene glycol (EG) poisoning is among a common toxic poisoning. The toxicity of EG is mediated by its metabolites. It can cause AKI or may progress to CKD. Treatments of EG poisoning consist of supportive care, fomepizole or ethanol and hemodialysis (HD). However, there are no definite guidelines on HD treatment. According to literatures, HD can be required if there are signs such as severe metabolic acidosis, hemodynamic instability and renal dysfunction. Herein, we report the unusual clinical course of a patient presenting with AKI in acute EG poisoning. A 77-year-old male visited emergent department after drinking two cups of EG. Laboratory data showed followings: serum creatinine, 0.8 mg/ dL; serum bicarbonate, 22.0 mM/L. But, his laboratory data on 5 days after treatments, including lavage, ingestion of alcohol and saline, deteriorated: serum creatinine and bicarbonate; 5.2 mg/dL and 14.4 mM/L; crystalluria, 4+. His vital signs were unstable and he showed oliguria. The oliguric AKI initiated to recovery after CRRT and HD during two weeks. After 2months, the renal function was restored with only HD once a week, but there was no complete recovery. Renal biopsy performed to identify irreversibility of renal injury showed severe tubular necrosis with crystal deposition consistent with calcium oxalate. Eventually, the severe renal injury progressed to ESRD after only 3 months, which required HD three time a week. Since renal toxicity appears about 24 to 72 hours after EG poisoning, clinical manifestations of acute EG poisoning in emergent department can be underestimated. Also, EG assay are seldom available. The metabolites of EG result in nephrotoxicity, so rapid elimination of metabolites via extracorporeal dialysis such as HD can be helpful to prevent progression of AKI. This case illustrates that the rapid decision of HD initiation may be helpful for favorable renal prognosis in acute EG poisoning setting. Urine smear and Light microscopic findings for acute oxalate nephropathy combined with acute tubular necrosis