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Abstract: TH-PO0100

A Rare Case of Metformin-Associated Lactic Acidosis with Concurrent Euglycemic Ketoacidosis in a Patient with Type 2 Diabetes

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Adnani, Harsha, University of Maryland Baltimore, Baltimore, Maryland, United States
  • Ladiwala, Zoya Fatima Rizwan, University of Maryland Baltimore, Baltimore, Maryland, United States
  • Pournazari, Kamyar, University of Maryland Baltimore, Baltimore, Maryland, United States
  • Lee, Melinda S, University of Maryland Baltimore, Baltimore, Maryland, United States
  • Patel, AMi, University of Maryland Baltimore, Baltimore, Maryland, United States
  • King, Joshua D., University of Maryland Baltimore, Baltimore, Maryland, United States
Introduction

Metformin-associated lactic acidosis (MALA) is a rare life-threatening complication with a mortality rate of 30-50%. Euglycemic diabetic ketoacidosis (euDKA) is increasingly seen with sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) use. This case involves severe MALA with concurrent euDKA requiring urgent renal replacement therapy (RRT).

Case Description

A 59-year-old African American female with type 2 diabetes (on metformin 1 g twice daily and a GLP-1 RA), hypertension (on valsartan), and stage 3A chronic kidney disease (CKD) (baseline creatinine 1.2 mg/dL) presented with three days of vomiting, abdominal pain, and acute vision loss after caring for sick grandchildren. The patient had doubled her metformin dosage after initial emesis.
On examination, the patient was hypothermic, hypotensive (84/52 mmHg) and tachypneic. Lab work revealed severe metabolic acidosis (pH 6.87, bicarbonate <5 mEq/L), hyperkalemia (7.1 mEq/L), acute kidney injury (creatinine 10.54 mg/dL), lactic acidosis (>17 mmol/L), and evidence of ketoacidosis (ketonuria, beta-hydroxybutyrate 30 mg/dL). The measured metformin level was approximately 17 μg/mL (therapeutic 0-5 ug/mL).
The patient was initiated on bicarbonate and insulin infusions. Emergent hemodialysis with vasopressors was commenced, followed by continuous veno-venous hemodiafiltration (CVVHDF) at high dose (6L/hr replacement fluid) with bicarbonate pre-blood pump infusion at 150cc/hr. Lactate levels decreased from >17 to 3.9 mmol/L within 48 hours. RRT was discontinued after 24 hours. Two weeks post-discharge, creatinine decreased to 1.8 mg/dL and later returned to baseline of 1.2 mg/dL.

Discussion

This case underscores the development of severe anion-gap metabolic acidosis due to combined effects of MALA and euDKA, likely triggered by ongoing metformin use in the setting of acute kidney injury from volume depletion, underlying CKD, and RAAS inhibitor therapy. MALA occurs when metformin accumulates, as in AKI, and inhibits mitochondrial complex I, shifting pyruvate metabolism toward lactate production. Prompt and intensive RRT; beginning with high-flux hemodialysis and followed by high-dose CVVHDF with bicarbonate pre blood pump is effective in correcting acidemia and eliminating metformin.

Digital Object Identifier (DOI)