Mediators of inflammation in acute kidney injury.
Acute kidney injury (AKI) remains to be an independent risk factor for mortality and morbidity. Inflammation is now believed to play a major role in the pathophysiology of AKI. It is hypothesized that in ischemia, sepsis and nephrotoxic models that the initial insult results in morphological and/or functional changes in vascular endothelial cells and/or in tubular epithelium. Then, leukocytes including neutrophils, macrophages, natural killer cells, and lymphocytes infiltrate into the injured kidneys. The injury induces the generation of inflammatory mediators like cytokines and chemokines by tubular and endothelial cells which contribute to the recruiting of leukocytes into the kidneys. Thus, inflammation has an important role in the initiation and extension phases of AKI. This review will focus on the mediators of inflammation contributing to the pathogenesis of AKI.
Akcay
Ali
A
Division of Renal Diseases and Hypertension, University of Colorado Denver, Aurora, CO 80262, USA.
Nguyen
Quocan
Q
Edelstein
Charles L
CL
D058186:Acute Kidney Injury / Q000401:mortality / Q000473:pathology / Q000503:physiopathology*; D015815:Cell Adhesion Molecules / Q000378:metabolism; D018925:Chemokines / Q000276:immunology; D003165:Complement System Proteins / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D004721:Endoplasmic Reticulum / Q000378:metabolism; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism*; D007684:Kidney Tubules / Q000378:metabolism / Q000473:pathology; D013312:Stress, Physiological; D051193:Toll-Like Receptors / Q000276:immunology
D015815:Cell Adhesion Molecules; D018925:Chemokines; D016207:Cytokines; D018836:Inflammation Mediators; D051193:Toll-Like Receptors; D003165:Complement System Proteins