Abstract: PUB101
SGLT2 Inhibitor-Triggered AKI Precipitating Metformin-Associated Lactic Acidosis: A Case Report
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Jun, Jae Hyun, Daejeon Eulji University Hospital, Seo-gu, Daejeon, Korea (the Republic of)
- Hwang, Seok Jin, Daejeon Eulji University Hospital, Seo-gu, Daejeon, Korea (the Republic of)
- Lee, Sua, Hallym University Kangnam Sacred Heart Hospital, Yeongdeungpo-gu, Seoul, Korea (the Republic of)
Introduction
Metformin-associated lactic acidosis (MALA) is a rare but potentially fatal complication arising from metformin accumulation due to impaired renal clearance. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) confer cardiorenal benefits; however, osmotic diuresis and natriuresis can precipitate volume depletion and acute kidney injury (AKI). We report a case in which SGLT2i initiation triggered AKI leading to life-threatening MALA in a metformin-treated patient with chronic kidney disease (CKD).
Case Description
A 78-year-old woman with type 2 diabetes mellitus and CKD presented with progressive generalized edema over five months. Medications included metformin 1,000 mg/day, linagliptin 2.5 mg/day, and lobeglitazone 0.5 mg/day. Furosemide 40 mg/day was added for volume management, and empagliflozin was initiated for renoprotection (baseline creatinine [Cr] 1.26 mg/dL; urine protein/creatinine 0.334 mg/mg).
Two days later, she was admitted with loss of consciousness (blood pressure 122/46 mmHg, heart rate 104 beats/min). Laboratory findings revealed Cr 6.37 mg/dL, arterial pH 7.03, PaCO2 32 mmHg, bicarbonate 8.5 mmol/L, lactate 167.4 mg/dL (reference <18 mg/dL), and anion gap 33.3 mEq/L, confirming severe high anion gap metabolic acidosis consistent with MALA. Pre-renal AKI from combined furosemide and SGLT2i-related dehydration was suspected, with metformin accumulation deemed responsible for the lactic acidosis. Continuous kidney replacement therapy (CKRT) was promptly initiated for metabolic rescue and renal support.
Within 24 hours of CKRT, lactate declined to 16.3 mg/dL and Cr improved to 2.67 mg/dL. CKRT was discontinued at 48 hours, and the patient was discharged with Cr stabilized at 1.38 mg/dL.
Discussion
SGLT2i initiation can precipitate AKI and trigger MALA in metformin-treated CKD patients, particularly with concurrent diuretic use and advanced age. Proactive risk assessment—including temporary metformin suspension and serial renal function monitoring during SGLT2i initiation—is essential to prevent this life-threatening complication.