Acute kidney injury (AKI) is a common complication of cardiac surgery and its occurrence is associated with increased risk of all-cause mortality, adverse cardiovascular outcomes, and chronic kidney disease (CKD).1 Mitochondria are essential for healthy function of the kidneys owing to their roles in oxidative phosphorylation, reactive oxygen species generation, and programmed cell death.2 Experimental evidence suggests that mitochondrial dysfunction is a key contributor to the pathophysiology of AKI and that replenishment of mitochondrial stores is necessary for recovery from AKI,3-5 but limited data exist in humans.