Case Presentation: A 76-year-old woman with hypertension, hyperlipidemia, and type 2 diabetes on metformin presented with seven days of nausea, vomiting, and diarrhea. She had no recent travel, antibiotic use, or sick contacts. On arrival, she was hypotensive and clinically hypovolemic. Laboratory results showed BUN 78 mg/dL, creatinine 7.08 mg/dL (GFR 6 mL/min/1.73 m²), bicarbonate 5 mmol/L, anion gap 28, phosphate 10.7 mg/dL, and lactate 24 mmol/L. Arterial blood gas demonstrated pH 6.8, pCO₂ 26 mmHg, and bicarbonate 11.9 mmol/L, confirming severe anion gap metabolic acidosis with concurrent respiratory acidosis.Given her gastrointestinal losses and hypovolemia, she was initially thought to have prerenal AKI progressing toward ischemic acute tubular necrosis. The presence of ketosis and an elevated anion gap suggested starvation ketoacidosis, and she was started on an insulin drip and intravenous bicarbonate in dextrose. However, despite resuscitation and resolution of hypotension, lactate remained markedly elevated, prompting reconsideration of the diagnosis. Her severe AKI had impaired metformin clearance, leading to metformin-associated lactic acidosis (MALA), a rare but life-threatening cause of Type B lactic acidosis. She underwent urgent hemodialysis with gradual clinical and metabolic recovery.
Discussion: Metformin, a biguanide and first-line therapy for diabetes, increases plasma lactate by inhibiting hepatic mitochondrial respiration. In the absence of a secondary insult, this effect is minimal. However, when lactate clearance is impaired, most commonly by acute kidney injury, sepsis, or hypoxia, metformin accumulation can precipitate Type B lactic acidosis. MALA is rare, with fewer than 10 cases per 100,000 patients, yet carries a mortality rate of nearly 50%.In this case, hypovolemia-induced AKI served as the precipitating factor, allowing metformin to accumulate and trigger severe lactic acidosis. The degree of acidemia and lactate elevation was disproportionate to typical starvation ketoacidosis, prompting reevaluation of the diagnosis. Early recognition of this overlap is critical, as MALA requires prompt discontinuation of metformin and emergent hemodialysis to remove both lactate and the offending agent.
Conclusions: MALA should be suspected in patients with diabetes and renal dysfunction who present with severe, persistent lactic acidosis unexplained by hypoperfusion or hypoxia. Recognizing this condition early and initiating hemodialysis can be lifesaving. Careful medication review and consideration of drug-induced metabolic disturbances are essential when evaluating complex acid–base disorders.