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

Abstract

Methanol intoxication is a potentially lethal condition that primarily affects the central nervous system, but it can also induce significant renal damage. Acute kidney injury (AKI) in this context is often underestimated, despite being an important prognostic marker associated with increased mortality and morbidity. This review aims to elucidate the pathophysiological mechanisms linking methanol intoxication to AKI, describe the cellular and metabolic pathways involved, and discuss current therapeutic approaches for renal protection and recovery. A descriptive and analytical review was conducted through searches in the PubMed, Embase, and Cochrane Library databases, including studies published between 2000 and 2025. Eligible articles addressed methanol-related nephrotoxicity, AKI mechanisms, or treatment strategies involving fomepizole, hemodialysis, and renal support. The nephrotoxic effects of methanol are mediated by the accumulation of formic acid, which inhibits mitochondrial cytochrome oxidase, leading to tissue hypoxia, oxidative stress, and cellular apoptosis. The main renal alterations include osmotic nephrosis and acute tubular necrosis, frequently associated with metabolic acidosis, rhabdomyolysis, or hemolysis. Risk factors such as anemia, sepsis, volume depletion, and acute pancreatitis exacerbate renal injury. AKI is linked to higher rates of multiple organ failure and in-hospital mortality. Methanol-induced AKI results from multifactorial mechanisms involving mitochondrial dysfunction, oxidative stress, and hemodynamic instability.