Abstract Sepsis often leads to widespread injury causing multiple organ dysfunction and the development of AKI in sepsis often portends poor prognosis. The pathophysiology of sepsis induced AKI is complex and multifactorial. Initially it was thought that hypotension causing hypoperfusion of kidneys as the major cause of AKI in sepsis. Recent work has been shown that rather than hypoperfusion, microvascular dysfunction with release of inflammatory mediators, cytokines, microparticles with adaptation of tubular cells as the major contributor of sepsis induced AKI. The aim of this review is to focus on the recent advances in pathophysiology of sepsis induced AKI and understanding these complex mechanisms which may pave the way for newer treatments in the future which are directed against the specific pathophysiological mechanisms.