Abstract
Acute kidney injury (AKI) is a serious and common clinical condition characterized by a sudden decline in kidney function. Although kidney function decline is typically reversible, a certain subset of AKI patients eventually develop chronic kidney disease (CKD) and kidney failure. Immune cells are well-known mediators of injury sequelae. Myeloid cells such as neutrophils, dendritic cells, and macrophages drive the initial inflammatory response following AKI but can change their phenotype after resolution of the injury to promote repair. Failure to resolve the initial injury, or improper tubular repair, drives persistent myeloid cell accumulation that can result in the development of kidney fibrosis and CKD. In this review, we focus on the role of myeloid cells following AKI including the mechanisms through which they promote injury and repair.