Is the Renal Protective Effect of Montelukast on Vancomycin due to Its Antiallergic Mechanism?

We were particularly intrigued by Teran et al.'s findings that montelukast, a cysteinyl leukotriene receptor antagonist (LTRA), reduced vancomycin-associated acute kidney injury (AKI) in preclinical/clinical models.The cotreatment group showed elevated antioxidant markers like heme oxygenase-1 (HO-1) compared to vancomycin alone.Mechanistically, montelukast activated the p62/KEAP1/NRF2 pathway, enhancing HO-1-dependent antioxidant defenses[1].This aligns with Kan et al.'s review, which links vancomycin nephrotoxicity to oxidative stress, mitochondrial dysfunction, DNA damage, and apoptosis in renal tubular cells[2], supporting the "antioxidant" renoprotective mechanism.We hypothesize that the antiallergic properties of montelukast may work together with its ability to protect the kidneys.This idea is based on its known pharmacological action of reducing inflammatory responses driven by leukotrienes, which could intersect with the pathways that lead to kidney injury from vancomycin.Acute kidney injury (AKI) associated with vancomycin has been linked to oxidative stress and direct damage to kidney tubules [2].However, studies suggest that hypersensitivity reactions, which can be mediated by specific IgE or T-cell responses, may