Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11338
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dc.contributor.authorBellomo, Rinaldoen
dc.contributor.authorWan, Lien
dc.contributor.authorLangenberg, Christophen
dc.contributor.authorIshikawa, Kenen
dc.contributor.authorMay, Clive Nen
dc.date.accessioned2015-05-16T00:55:41Z-
dc.date.available2015-05-16T00:55:41Z-
dc.date.issued2011-09-09en
dc.identifier.citationContributions To Nephrology 2011; 174(): 98-107en
dc.identifier.govdoc21921614en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/11338en
dc.description.abstractAcute 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.en
dc.language.isoenen
dc.subject.otherAcute Kidney Injury.etiology.physiopathologyen
dc.subject.otherAnimalsen
dc.subject.otherArginine Vasopressin.pharmacologyen
dc.subject.otherArterioles.physiopathologyen
dc.subject.otherGlomerular Filtration Rateen
dc.subject.otherHumansen
dc.subject.otherKidney Glomerulus.blood supplyen
dc.subject.otherRenal Circulationen
dc.subject.otherSepsis.complicationsen
dc.titleSeptic acute kidney injury: the glomerular arterioles.en
dc.typeJournal Articleen
dc.identifier.journaltitleContributions to nephrologyen
dc.identifier.affiliationDepartment of Intensive Care, Austin Health, University of Melbourne, Melbourne, Australiaen
dc.identifier.doi10.1159/000329246en
dc.description.pages98-107en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/21921614en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptIntensive Care-
crisitem.author.deptData Analytics Research and Evaluation (DARE) Centre-
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