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Metformin-associated lactic acidosis risk — ABIM Board MCQ

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ModerateGeneral Internal MedicineMetformin-associated lactic acidosis riskABIM Board

A 70-year-old man with type 2 diabetes and chronic kidney disease takes metformin. He is admitted with septic shock and develops oliguric acute kidney injury. His serum lactate concentration is 8 mmol/L, and arterial pH is 7.18. Metformin is discontinued. Which mechanism best explains why the acute kidney injury increases the risk that metformin contributes to his lactic acidosis?

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Correct answer: D — Decreased renal elimination of metformin

The correct answer is D. Metformin is substantially eliminated by the kidneys. Acute kidney injury reduces its renal clearance, allowing drug accumulation and increasing the risk of metformin-associated lactic acidosis. Metformin impairs mitochondrial oxidative metabolism and hepatic lactate utilization; septic shock simultaneously increases lactate production through tissue hypoperfusion, so the acidosis may be multifactorial rather than attributable solely to metformin. Increased proximal tubular glucose reabsorption does not cause metformin accumulation. Metformin suppresses rather than increases hepatic gluconeogenesis from lactate and does not stimulate pancreatic insulin secretion. Increased renal bicarbonate generation would oppose metabolic acidosis and is impaired, not enhanced, in severe acute kidney injury.

Reference: US Food and Drug Administration. ZITUVIMET (sitagliptin and metformin hydrochloride), Full Prescribing Information, section 5.1, Metformin-Associated Lactic Acidosis. 2026. https://www.accessdata.fda.gov/drugsatfda_docs/label/2026/216743Orig1s005lbl.pdf