Metformin-Induced Lactic Acidosis: A Case Study

Chowdhury, Waliul; Lodhi, Muhammad Uzair; Syed, Intekhab Askari; Ahmed, Umer; Miller, Maxwell; Rahim, Mustafa

doi:10.7759/cureus.2152

Cited by 4 publications

(5 citation statements)

References 8 publications

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“…This is a case where a patient was being treated with the recommended Met dose and presented at the emergency unit and was diagnosed with AKI. PK analysis revealed that AKI might be caused by high plasma Met levels, consistent with previous reports that have demonstrated that Met overdose causes AKI [ 7 – 9 ]. Possible mechanism to cause AKI by Met is the decrement of mitochondrial adenosine triphosphate (ATP) by Met [ 10 ] since AKI can arise from mitochondrial ATP depletion [ 11 ].…”

Section: Discussionsupporting

confidence: 90%

“…This high Met concentration occurred in a patient who attempted suicide by taking 26,250 mg of Met (42.9 µg/mL at admission); this patient displayed acute tubular necrosis [ 7 ]. In the case a person without renal dysfunction overdosed on Met, he presented with high Met concentrations and consequently with AKI [ 9 ]. These results suggest that high Met concentrations possibly cause AKI.…”

Section: Discussionmentioning

confidence: 99%

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Daily dose of metformin caused acute kidney injury with lactic acidosis: a case report

Ariga,

Hagita,

Soda

et al. 2023

J Med Case Reports

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Background Metformin-induced lactic acidosis with acute kidney injury is rare but well known. Here we report a case of a Japanese patient taking metformin who experienced severe acute renal failure accompanied with significantly elevated metformin plasma concentrations and signs of lactic acidosis. Case presentation A 60-year-old Japanese man with type II diabetes, who was taking metformin (500 mg three times a day) along with several other medications, visited the emergency department with dizziness, malaise, and oliguria. The initial laboratory test results showed elevated levels of serum creatinine and blood urea nitrogen, although his renal function was normal approximately 2 weeks earlier. His lactate level was raised (4.27 mmol/L), and he was diagnosed with lactic acidosis. Considering the low creatinine clearance and elevated urinary albumin/serum creatinine ratio, urinary N-acetyl-β-d-glucosaminidase level, and β2-microglobulin level, the patient was further diagnosed with AKI (in other words, acute tubular necrosis). A renal biopsy performed on day 3 after admission revealed renal tubular epithelium necrosis, supporting this diagnosis. The patient underwent intermittent hemodialysis until he was discharged on day 13. The metformin concentrations on days 3, 5, and 7 were 8.95, 2.58, and 0.16 μg/mL, respectively, which is significantly higher than the maximal steady-state concentration of metformin at the recommended dosage (approximately 1 μg/mL). The calculated pharmacokinetic parameters of metformin suggested poor renal excretion and a low distribution volume at higher metformin levels. Other possible acute kidney injury-causing factors included dehydration, alcohol consumption, and the use of an angiotensin receptor blocker or SGLT2 inhibitor. Conclusions This is the first reported case of acute kidney injury possibly caused by high levels of metformin with lactic acidosis in a patient treated with the recommended metformin dose. Thus, the development of metformin-induced acute kidney injury should be considered for patients with several acute kidney injury risk factors who are taking metformin.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Daily dose of metformin caused acute kidney injury with lactic acidosis: a case report

Ariga,

Hagita,

Soda

et al. 2023

J Med Case Reports

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“…Hence, Metformin ingestion should always be considered in the differential diagnoses of any patient with metabolic acidosis and high lactate level. (22,23). Activated charcoal should be considered in patients who present soon after ingestion, provided that there are no contraindications (10,26).…”

Section: Discussionmentioning

confidence: 99%

Severe Metformin poisoning; Experience at a tertiary care hospital in Sri Lanka: a case series

Sirisena¹,

Hettiarachchi²,

Manilgama

et al. 2022

Asian J. Internal Med.

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Metformin is the first line medication used for the treatment of type 2 diabetes mellitus worldwide. It has been considered a cost effective and safe drug for decades. Though, lactic acidosis is a recognized adverse effect of metformin, it is sparsely seen with therapeutic doses. However, it occurs frequently in patients with metformin overdose and in the presence of renal insufficiency. Metformin associated lactic acidosis (MALA) carries a mortality rate of almost 50%. Early initiation of renal replacement therapy has shown to reduce morbidity and mortality in these patients. Metformin overdose is relatively uncommon and only few cases of severe metformin overdose are reported in the literature. Here, we discuss five cases of MALA due to severe metformin poisoning. Four of them were successfully treated with early use of renal replacement therapy.

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“…However, metformin-induced metabolic acidosis, which is a serious complication with a mortality rate of 50%, may rarely occur. This complication is known to be associated with lactic acid elevation [3].…”

Section: Introductionmentioning

confidence: 99%

An Unexpected Complication Due to Metformin Use After Femur Fracture Operation: Metabolic Acidosis Without Lactic Acidosis

Yaşar

Altıparmak

Demirbilek

2019

Cureus

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A 74-year- old male, who was known to have hypertension, chronic obstructive lung disease, and benign prostate hyperplasia, was evaluated preoperatively in our clinic for a femur fracture. In addition, it was found that the patient was using 1000 mg of metformin per oral due to type 2 diabetes. At the preoperative cardiology evaluation, the ejection fraction was 60% with normal systolic ventricular function. Routine laboratory tests were normal. Metformin was held 24 hours before surgery. Spinal anesthesia was applied with 10 mg bupivacaine and 20 mcg fentanyl. Total blood loss at surgery was 150 cc. After an uneventful surgery, the patient was observed at the surgical postanesthesia care unit. Cardiac and respiratory physical examinations seemed normal but the patient had minimal acidosis and hypoxia in the arterial blood gas analysis. Twelve hours after the operation, compensated high anion gap ( 30 mEq/l) metabolic acidosis emerged, but lactate was normal. The patient's urea and creatinine levels were normal in the control blood tests, and the patient's urine output was above 0.5 ml/kg. Within this period, glucose levels were around 80-140 mg/dl. To overcome metabolic acidosis, bolus intravenous 8.4 % bicarbonate solution was administered. Bicarbonate infusion was started on the continuation of metabolic acidosis and base loss despite the bolus bicarbonate treatment. Since there was no other reason for the metabolic acidosis, metformin usage was considered to cause metabolic acidosis. During this treatment period, despite high anion gap acidosis, there was no lactate elevation. The patient had normal laboratory and hemodynamic values and was discharged from the intensive care unit at postoperative Day 3.

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Metformin-Induced Lactic Acidosis: A Case Study

Cited by 4 publications

References 8 publications

Daily dose of metformin caused acute kidney injury with lactic acidosis: a case report

Daily dose of metformin caused acute kidney injury with lactic acidosis: a case report

Severe Metformin poisoning; Experience at a tertiary care hospital in Sri Lanka: a case series

An Unexpected Complication Due to Metformin Use After Femur Fracture Operation: Metabolic Acidosis Without Lactic Acidosis

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