Pathogenesis of Acute Kidney Injury

Abstract

The rapid loss of kidney function that results from renal ischemia-, sepsis-, toxic-, or toxicant-induced renal cell injury is termed acute kidney injury (AKI). The operative word “injury” initially referred primarily to renal tubule cell injury. However, it has since become clear that the expanse of cellular alterations and injury is broad, affecting other types of cells resident in the kidney that are central to the pathophysiology of AKI. This chapter focuses on the pathophysiology of AKI triggered by an ischemic insult as revealed in experimental models both in vivo and in vitro. How mechanisms of sepsis-induced AKI, a principal cause of AKI in children, overlap with and differ from ischemia-induced AKI is discussed. Included are classical concepts of acute tubular necrosis as well as a contemporary understanding of vascular, cellular, molecular, inflammatory, and metabolic alterations that are associated with renal cell injury. Mechanisms that lead to cell injury and death are addressed along with processes that can result in cellular repair and renal recovery.