Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/11022
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.
Issue Date: 20-Apr-2010
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
URI: http://ahro.austin.org.au/austinjspui/handle/1/11022
DOI: 10.1159/000313740
URL: http://www.ncbi.nlm.nih.gov/pubmed/20427951
Type: Journal Article
Subjects: Acute Kidney Injury.complications.pathology.physiopathology
Animals
Epithelial Cells.physiology
Humans
Inflammation.physiopathology
Leukocytes.physiology
Mice
Mice, Knockout
Reperfusion Injury.physiopathology
Sepsis.complications.physiopathology
Toll-Like Receptors.deficiency.physiology
Vasodilation.physiology
Appears in Collections:Journal articles

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