The multifaceted role of the renal microvasculature during acute kidney injury.
Pediatric acute kidney injury (AKI) represents a complex disease process for clinicians as it is multifactorial in cause and only limited treatment or preventatives are available. The renal microvasculature has recently been implicated in AKI as a strong therapeutic candidate involved in both injury and recovery. Significant progress has been made in the ability to study the renal microvasculature following ischemic AKI and its role in repair. Advances have also been made in elucidating cell-cell interactions and the molecular mechanisms involved in these interactions. The ability of the kidney to repair post AKI is closely linked to alterations in hypoxia, and these studies are elucidated in this review. Injury to the microvasculature following AKI plays an integral role in mediating the inflammatory response, thereby complicating potential therapeutics. However, recent work with experimental animal models suggests that the endothelium and its cellular and molecular interactions are attractive targets to prevent injury or hasten repair following AKI. Here, we review the cellular and molecular mechanisms of the renal endothelium in AKI, as well as repair and recovery, and potential therapeutics to prevent or ameliorate injury and hasten repair.
Rangos Research Center, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA, USA.|Division of Nephrology, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Katherine
K
Maringer
Rangos Research Center, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA, USA. simslucass@upmc.edu.|Division of Nephrology, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. simslucass@upmc.edu.|Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA, USA. simslucass@upmc.edu.
Sunder
S
Sims-Lucas
D058186:Acute Kidney Injury / Q000473:pathology*; D000818:Animals; D002648:Child; D006801:Humans; D007668:Kidney / Q000098:blood supply; D055806:Microvessels / Q000473:pathology*
Acute kidney injury; Endothelium; Immune response; Ischemia reperfusion injury; Microvasculature; Tissue hypoxia