The proximal tubule relies on oxidative mitochondrial metabolism to meet its energy needs
and has limited capacity for glycolysis, which makes it uniquely susceptible to damage
during AKI, especially after ischemia and anoxia. Under these conditions, mitochondrial ATP
production is initially decreased by several mechanisms, including fatty acid–induced
uncoupling and inhibition of respiration related to changes in the shape and volume of
mitochondria. Glycolysis is initially insufficient as a source of ATP to protect the cells and …