Pathophysiology of AKI: injury and normal and abnormal repair.
The pathophysiology of acute kidney injury involves a complex interplay among vascular, tubular, and inflammatory factors followed by a repair process that can either restore epithelial differentiation and function to normal or result in progressive fibrotic chronic kidney disease. Innate and acquired immunity play an important role in the injury phase, in the regulation of the inflammatory response, and in processes related to repair of the epithelial layer. Recent data change the direction of focus of the role of the epithelium in fibrosis and attributes myelofibroblast production to perivascular and interstitial fibroblasts. The epithelium plays an important role in abnormal repair through a recently defined link between cell cycle arrest of the epithelial cell and profibrogenic cytokine production.
Bonventre
Joseph V
JV
Renal Division, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, Boston, Mass., USA.
D058186:Acute Kidney Injury / Q000503:physiopathology*; D000818:Animals; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000502:physiology; D007668:Kidney / Q000293:injuries* / Q000473:pathology; D007684:Kidney Tubules / Q000503:physiopathology; D007962:Leukocytes / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D008871:Microvilli / Q000473:pathology; D012079:Renal Circulation / Q000502:physiology; D015427:Reperfusion Injury / Q000503:physiopathology; D014661:Vasoconstriction
D018799:Intercellular Adhesion Molecule-1