Severe lactic acidosis and hypoglycemia associated with progressive acute kidney injury during imeglimin therapy: a case report

Background Imeglimin is an oral antidiabetic agent for type 2 diabetes that is primarily excreted unchanged in the urine. Although the development of lactic acidosis has not been reported in clinical trials, clinical data regarding the safety of imeglimin in the setting of progressive acute kidney injury (AKI) remain limited. Case presentation A 46-year-old man was receiving imeglimin 1000 mg twice daily and teneligliptin 20 mg once daily for type 2 diabetes. Losartan was initiated on Day − 6, and contrast-enhanced computed tomography for preoperative evaluation was performed on Day − 5. On Day − 4, his serum creatinine level increased from a baseline of 0.77–0.84 mg/dL to 1.37 mg/dL; however, imeglimin was continued at the same dose. On Day − 1, he experienced nausea and hypoglycemia, leading to the discontinuation of both imeglimin and teneligliptin. On Day 0, he presented with a pH of 7.233, lactate level of 5.6 mmol/L, serum creatinine of 5.15 mg/dL, and blood glucose of 58 mg/dL. He was admitted to the intensive care unit for lactic acidosis, severe renal impairment, and hypoglycemia. Findings supporting recurrent infection, overt circulatory failure, hypoxemia, or liver failure were lacking. Treatment with continuous hemodiafiltration, glucose administration, and sodium bicarbonate improved the lactate level and corrected acidosis, hyperkalemia, and hypoglycemia. Conclusions Given the continuation of imeglimin despite the progression of AKI, increased imeglimin exposure due to renal deterioration may have contributed to the development of lactic acidosis and hypoglycemia. When acute changes in renal function occur, the continuation of renally excreted antidiabetic agents, including imeglimin, should be repeatedly reassessed throughout the clinical course.