Methanol intoxication and acute kidney injury: pathophysiological mechanisms and therapeutic approaches

Area of Science:

• Toxicology
• Nephrology
• Critical Care Medicine

Background:

• Methanol intoxication poses a life-threatening risk, primarily impacting the central nervous system.
• Renal damage, including acute kidney injury (AKI), is a significant but often underestimated complication of methanol poisoning.
• AKI in methanol intoxication is a critical prognostic indicator of increased mortality and morbidity.

Purpose of the Study:

• To review the pathophysiological mechanisms linking methanol intoxication to AKI.
• To describe the cellular and metabolic pathways involved in methanol-induced nephrotoxicity.
• To discuss current therapeutic strategies for renal protection and recovery in methanol poisoning.

Main Methods:

• A descriptive and analytical literature review was performed.
• Searches were conducted in PubMed, Embase, and Cochrane Library databases for studies published between 2000 and 2025.
• Eligible articles focused on methanol nephrotoxicity, AKI mechanisms, and treatments like fomepizole and hemodialysis.

Main Results:

• Methanol's nephrotoxicity is driven by formic acid accumulation, inhibiting mitochondrial function and causing hypoxia, oxidative stress, and apoptosis.
• Renal damage manifests as osmotic nephrosis and acute tubular necrosis, often co-occurring with metabolic acidosis, rhabdomyolysis, or hemolysis.
• Risk factors like anemia, sepsis, and pancreatitis worsen renal injury, correlating with higher rates of multiple organ failure and mortality.

Conclusions:

• Methanol-induced AKI stems from complex interactions including mitochondrial dysfunction, oxidative stress, and hemodynamic instability.
• Early recognition and management of AKI are vital for improving prognosis in methanol-intoxicated patients.
• Further research into targeted renal protective therapies is warranted.