Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11338
Title: Septic acute kidney injury: the glomerular arterioles.
Austin Authors: Bellomo, Rinaldo ;Wan, Li;Langenberg, Christoph;Ishikawa, Ken;May, Clive N
Affiliation: Department of Intensive Care, Austin Health, University of Melbourne, Melbourne, Australia
Issue Date: 9-Sep-2011
Publication information: Contributions To Nephrology 2011; 174(): 98-107
Abstract: Acute kidney injury (AKI) is a serious condition that affects many intensive care unit (ICU) patients. The most common causes of AKI in the ICU are severe sepsis and septic shock. The mortality of AKI in septic critically ill patients remains high despite our increasing ability to support vital organs. This is partly due to our poor understanding of the pathogenesis of sepsis-induced renal dysfunction. However, new concepts are emerging to explain the pathogenesis of septic AKI, which challenge previously held dogma. Throughout the past half century, septic AKI has essentially been considered secondary to tubular injury, which, in turn, has been considered secondary to renal ischemia. This belief is curious because the hallmark of septic AKI and AKI in general is the loss of glomerular filtration rate (GFR). It would seem logical, therefore, to focus on the glomerulus in trying to understand why such loss of GFR occurs. Recent experimental observations suggest that, at least in the initial phases of septic AKI, profound changes occur which involve glomerular hemodynamics and lead to loss of GFR. These observations imply that changes in the vasoconstrictor tone of both the afferent and efferent arterioles are an important component of the pathogenesis of septic AKI.
Gov't Doc #: 21921614
URI: https://ahro.austin.org.au/austinjspui/handle/1/11338
DOI: 10.1159/000329246
Journal: Contributions to nephrology
URL: https://pubmed.ncbi.nlm.nih.gov/21921614
Type: Journal Article
Subjects: Acute Kidney Injury.etiology.physiopathology
Animals
Arginine Vasopressin.pharmacology
Arterioles.physiopathology
Glomerular Filtration Rate
Humans
Kidney Glomerulus.blood supply
Renal Circulation
Sepsis.complications
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