Novel therapeutic targets for prevention and therapy of sepsis associated acute kidney injury.
Sepsis associated Acute Kidney Injury (SA-AKI) is the leading cause of AKI in the hospital setting and its incidence is increasing. Although the exact pathophysiology and phenotype of SA-AKI are not known, it is widely accepted that SA-AKI has a multi-injury pathway. This form of AKI has components of ischemia-reperfusion injury, direct inflammatory injury, coagulation and endothelial cell dysfunction, and apoptosis. As such, multiple agents have been shown in pre-clinical studies to ameliorate SA-AKI, but there are no interventions currently available for the treatment of SA-AKI. Promising agents that are in development include toll-like receptor inhibition, IL-10 augmentation, modulators of the protein C pathway, and mesenchymal stem cell mediated therapeutics. The aim of this review is to review the pathophysiology of SA-AKI and the therapeutic interventions that are under development to treat this complex and morbid disease.
Pelte
Christian H
CH
Department of Anesthesiology and Critical Care Medicine, Washington, DC 20037, USA.
Chawla
Lakhmir S
LS
D058186:Acute Kidney Injury / Q000188:drug therapy* / Q000209:etiology / Q000517:prevention & control*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D042783:Endothelial Cells / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000473:pathology; D018836:Inflammation Mediators / Q000502:physiology; D012079:Renal Circulation; D015427:Reperfusion Injury / Q000188:drug therapy / Q000517:prevention & control; D018805:Sepsis / Q000150:complications / Q000188:drug therapy* / Q000517:prevention & control*; D051193:Toll-Like Receptors / Q000502:physiology
D018836:Inflammation Mediators; D051193:Toll-Like Receptors