Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10579
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dc.contributor.authorWan, Lien
dc.contributor.authorBagshaw, Sean Men
dc.contributor.authorLangenberg, Christophen
dc.contributor.authorSaotome, Takaoen
dc.contributor.authorMay, Clive Nen
dc.contributor.authorBellomo, Rinaldoen
dc.date.accessioned2015-05-16T00:05:00Z
dc.date.available2015-05-16T00:05:00Z
dc.date.issued2008-04-01en
dc.identifier.citationCritical Care Medicine; 36(4 Suppl): S198-203en
dc.identifier.govdoc18382194en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10579en
dc.description.abstractSeptic acute kidney injury accounts for close to 50% of all cases of acute kidney injury in the intensive care unit and, in its various forms, affects between 15% and 20% of intensive care unit patients. However, there is little we really know about its pathophysiology. Although hemodynamic factors might play a role in the loss of glomerular filtration rate, they may not act through the induction of renal ischemia. Septic acute renal failure may, at least in patients with a hyperdynamic circulation, represent a unique form of acute renal failure: hyperemic acute renal failure. Measurements of renal blood flow in septic humans are now needed to resolve this pivotal pathophysiological question. Whatever may happen to renal blood flow during septic acute kidney injury in humans, the evidence available suggests that urinalysis fails to provide useful diagnostic or prognostic information in this setting. In addition, nonhemodynamic mechanisms of cell injury are likely to be at work. These mechanisms are likely due to a combination of immunologic, toxic, and inflammatory factors that may affect the microvasculature and the tubular cells. Among these mechanisms, apoptosis may turn out to be important. It is possible that, as evidence accumulates, the paradigms currently used to explain acute renal failure in sepsis will shift from ischemia and vasoconstriction to hyperemia and vasodilation and from acute tubular necrosis to acute tubular apoptosis or simply tubular cell dysfunction or exfoliation. If this were to happen, our therapeutic approaches would also be profoundly altered.en
dc.language.isoenen
dc.subject.otherAcute Kidney Injury.etiology.physiopathologyen
dc.subject.otherHemodynamicsen
dc.subject.otherHumansen
dc.subject.otherLogistic Modelsen
dc.subject.otherRenal Circulationen
dc.subject.otherSepsis.complications.physiopathologyen
dc.titlePathophysiology of septic acute kidney injury: what do we really know?en
dc.typeJournal Articleen
dc.identifier.journaltitleCritical Care Medicineen
dc.identifier.affiliationDepartment of Intensive Care, Austin Hospital, Melbourne, Australiaen
dc.identifier.doi10.1097/CCM.0b013e318168ccd5en
dc.description.pagesS198-203en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/18382194en
dc.type.austinJournal Articleen
item.fulltextNo Fulltext-
item.openairetypeJournal Article-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptIntensive Care-
crisitem.author.deptData Analytics Research and Evaluation (DARE) Centre-
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