Sepsis is the most common cause of acute kidney injury (AKI) among critically ill patients. Importantly, sepsis-induced AKI greatly increases the risk of death and progression to chronic kidney disease among survivors. The complex mechanisms of septic AKI was not well studied which seriously impedes the development of specific prevention and treatment strategies. Recent evidence showed that microvascular dysfunction, adaptive responses of tubular epithelial cells and in?mmation played critical role in the pathogenesis of sepsis-induced AKI. Therefore, in this review, we focus on the advances in fundamental pathophysiology of sepsis-induced AKI and provide useful information and novel ideas to clinicians and researchers for future studies.