Severe Suspected Metformin-Associated Lactic Acidosis With Relatively Preserved Serum Creatinine at Presentation: Sequential Intermittent Hemodialysis and Continuous Venovenous Hemodialysis.
- 1Nephrology, SSM (Sisters of St. Mary) Health Saint Louis University Hospital, St. Louis, USA.
- 2Dialysis Services, SSM (Sisters of St. Mary) Health Saint Louis University Hospital, St. Louis, USA.
- 3Nephrology, SSM (Sisters of St. Mary) Health Saint Louis University Hospital Transplant Center, St. Louis, USA.
Abstract
Metformin-associated lactic acidosis (MALA) is an uncommon but potentially fatal complication of metformin therapy in which extracorporeal treatment may be required for severe acidemia or markedly elevated lactate levels. We report the case of a 47-year-old man with type 2 diabetes mellitus treated with metformin who presented with encephalopathy, profound hypoglycemia, hypothermia, and severe high-anion-gap metabolic acidosis. Lactate was 24.1 mmol/L and peaked at 25.5 mmol/L, while serum total carbon dioxide was <5 mmol/L. Despite the severity of the metabolic disturbance, serum creatinine was 1.18 mg/dL on presentation, although he had experienced recent acute kidney injury. Toxicologic evaluation did not identify an alternative major cause of the acidosis, although urine testing was positive for amphetamine/methamphetamine, suggesting a potentially multifactorial process. The patient received supportive care and repeated intravenous sodium bicarbonate before extracorporeal treatment. Lactate had already declined from 25.5 to 16.0 mmol/L before dialysis began, while acidemia partially improved after bicarbonate administration. High-efficiency intermittent hemodialysis (iHD) was initiated for severe suspected MALA as the rapid initial phase of extracorporeal treatment, followed by continuous venovenous hemodialysis to provide sustained therapy toward biochemical treatment targets; hemodynamic intolerance during iHD further supported the transition. Lactate subsequently normalized without rebound, and kidney function recovered without further renal replacement therapy. This case highlights that severe suspected MALA may warrant extracorporeal treatment despite relatively preserved creatinine at presentation and illustrates the importance of aligning biochemical trends with treatment timing when assessing the contribution of dialysis to lactate and acid-base correction.
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BibTeX
@article{hassanein2026severe,
title = {{Severe Suspected Metformin-Associated Lactic Acidosis With Relatively Preserved Serum Creatinine at Presentation: Sequential Intermittent Hemodialysis and Continuous Venovenous Hemodialysis.}},
author = {Mahmoud Hassanein and Christina Rodriguez and Krista L Lentine},
journal = {Cureus},
year = {2026},
month = sep,
doi = {10.7759/cureus.116607},
url = {https://europepmc.org/article/MED/42903999},
note = {CC BY},
}
RIS
TY - JOUR
TI - Severe Suspected Metformin-Associated Lactic Acidosis With Relatively Preserved Serum Creatinine at Presentation: Sequential Intermittent Hemodialysis and Continuous Venovenous Hemodialysis.
AU - Mahmoud Hassanein
AU - Christina Rodriguez
AU - Krista L Lentine
PY - 2026
DA - 2026/09/20
JO - Cureus
DO - 10.7759/cureus.116607
UR - https://europepmc.org/article/MED/42903999
AB - Metformin-associated lactic acidosis (MALA) is an uncommon but potentially fatal complication of metformin therapy in which extracorporeal treatment may be required for severe acidemia or markedly elevated lactate levels. We report the case of a 47-year-old man with type 2 diabetes mellitus treated with metformin who presented with encephalopathy, profound hypoglycemia, hypothermia, and severe high-anion-gap metabolic acidosis. Lactate was 24.1 mmol/L and peaked at 25.5 mmol/L, while serum total carbon dioxide was <5 mmol/L. Despite the severity of the metabolic disturbance, serum creatinine was 1.18 mg/dL on presentation, although he had experienced recent acute kidney injury. Toxicologic evaluation did not identify an alternative major cause of the acidosis, although urine testing was positive for amphetamine/methamphetamine, suggesting a potentially multifactorial process. The patient received supportive care and repeated intravenous sodium bicarbonate before extracorporeal treatment. Lactate had already declined from 25.5 to 16.0 mmol/L before dialysis began, while acidemia partially improved after bicarbonate administration. High-efficiency intermittent hemodialysis (iHD) was initiated for severe suspected MALA as the rapid initial phase of extracorporeal treatment, followed by continuous venovenous hemodialysis to provide sustained therapy toward biochemical treatment targets; hemodynamic intolerance during iHD further supported the transition. Lactate subsequently normalized without rebound, and kidney function recovered without further renal replacement therapy. This case highlights that severe suspected MALA may warrant extracorporeal treatment despite relatively preserved creatinine at presentation and illustrates the importance of aligning biochemical trends with treatment timing when assessing the contribution of dialysis to lactate and acid-base correction.
SN - 2168-8184
ER -