Please use this identifier to cite or link to this item:
|Title:||Pathophysiology of septic acute kidney injury: a different view of tubular injury.|
|Authors:||Ishikawa, Ken;May, Clive N;Gobe, Glenda;Langenberg, Christoph;Bellomo, Rinaldo|
|Affiliation:||Department of Intensive Care, Austin Health, Heidelberg, Melbourne, Australia.|
|Citation:||Contributions To Nephrology 2010; 165(): 18-27|
|Abstract:||Septic acute kidney injury (AKI) is the most common form of AKI seen in critically ill patients in developed countries. Its pathogenesis has been traditionally attributed to ischemia secondary to decreased cardiac output and hypotension, which trigger sustained renal vasoconstriction and in turn exacerbate and sustain the ischemia. This paradigm is supported by the fact that many patients who develop AKI do so in the setting of hemodynamic instability and also by evidence that renal blood flow is decreased and renal vascular resistance increased when they are measured in patients with AKI. However, recent evidence shows that renal blood flow may vary from increased in some animal models to normal in some patients and to decreased in other patients. Furthermore, the induction of prolonged severe subtotal ischemia by acute occlusion of the renal artery does not seem to trigger subsequent renal vasoconstriction and, finally, experimental studies suggest that immune-mediated injury may be a more likely cause of tubular cell dysfunction than ischemia. These lines of evidence suggest that the pathogenesis of AKI is complex, does not simply involve ischemia, and may differ according to the etiological trigger.|
|Internal ID Number:||20427951|
|Subjects:||Acute Kidney Injury.complications.pathology.physiopathology|
|Appears in Collections:||Journal articles|
Files in This Item:
There are no files associated with this item.
Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.