This leads to poor proximal handling of vancomycin, formation of uromodulin casts, increased local concentration of vancomycin, precipitation/ crystallization of vancomycin, and localized necrosis and damage of tubular epithelial cells, feed into a self-perpetuating positive feedback loop of local tubular injury, superimposing on the ATN and/or TIN-induced background AKI. This evidence concerns the gene UMOD and acute kidney injury.