Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11108
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dc.contributor.authorProwle, John Ren
dc.contributor.authorWesterman, Marken
dc.contributor.authorBellomo, Rinaldoen
dc.date.accessioned2015-05-16T00:41:44Z
dc.date.available2015-05-16T00:41:44Z
dc.date.issued2010-12-01en
dc.identifier.citationCurrent Opinion in Critical Care; 16(6): 540-4en
dc.identifier.govdoc20736824en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/11108en
dc.description.abstractIn this review, we discuss the potential role of urinary hepcidin, a 2.8-kDa hormonal regulator of iron metabolism, as a biomarker of acute kidney injury (AKI) after cardiopulmonary bypass.Hepcidin is one of the novel biomarkers of AKI that have been identified using hypothesis-free, proteomic analysis of urine or plasma in patients who develop AKI. Collectively, these markers promise a new era for the early diagnosis and treatment of AKI in the ICU and an understanding of their biological role may also provide mechanistic insights into the pathogenesis of AKI. Although data confirming the association between urinary hepcidin and AKI are as yet limited, we believe hepcidin is of particular interest because hepcidin may be a biomarker specific to cardiopulmonary bypass-associated AKI; as a central regulator of iron metabolism, hepcidin could play a biological role in the pathogenesis of AKI after cardiopulmonary bypass; and hepcidin displays an intriguing negative association with AKI, in that a smaller increase in hepcidin from baseline after cardiopulmonary bypass appears to predict greater chance of developing AKI.Smaller increases in urinary hepcidin, a central regulator of iron metabolism, may be associated with greater risk of AKI after cardiopulmonary bypass. Further research is required to establish the significance and nature of this association.en
dc.language.isoenen
dc.subject.otherAcute Kidney Injury.diagnosis.etiology.urineen
dc.subject.otherAcute-Phase Proteins.metabolismen
dc.subject.otherAntimicrobial Cationic Peptides.metabolism.urineen
dc.subject.otherBiological Markersen
dc.subject.otherCardiopulmonary Bypass.adverse effectsen
dc.subject.otherCritical Illnessen
dc.subject.otherHepcidinsen
dc.subject.otherHumansen
dc.subject.otherIron.metabolismen
dc.subject.otherLipocalins.metabolismen
dc.subject.otherPostoperative Complications.diagnosisen
dc.subject.otherProto-Oncogene Proteins.metabolismen
dc.subject.otherSensitivity and Specificityen
dc.titleUrinary hepcidin: an inverse biomarker of acute kidney injury after cardiopulmonary bypass?en
dc.typeJournal Articleen
dc.identifier.journaltitleCurrent opinion in critical careen
dc.identifier.affiliationjprowle@yahoo.co.uken
dc.identifier.affiliationDepartment of Intensive Care Medicine, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1097/MCC.0b013e32833ecdccen
dc.description.pages540-4en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/20736824en
dc.type.austinJournal Articleen
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.cerifentitytypePublications-
crisitem.author.deptIntensive Care-
crisitem.author.deptData Analytics Research and Evaluation (DARE) Centre-
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