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dc.contributor.advisorKennedy, Michael
dc.contributor.authorRuby, Hannah
dc.contributor.authorBashir, Sabina
dc.contributor.authorChihanga, Tafadzwa
dc.contributor.authorMa, Qing
dc.contributor.authorDevarajan, Prasad
dc.contributor.authorKennedy, Michael
dc.date.accessioned2017-06-13T14:57:49Z
dc.date.available2017-06-13T14:57:49Z
dc.identifier.urihttp://hdl.handle.net/2374.MIA/6133
dc.description.abstractAcute Kidney Injury (AKI) refers to the rapid decline of renal filtration and urine production due to functional and/or structural damage. Kidney damage is often due to sepsis, respiratory failure, heart failure, trauma, major surgery, burns, or toxic insult caused by medications. AKI can lead to severe complications, such as increased risk of chronic kidney disease and damage to other organ systems. Mortality associated with AKI is estimated at 45-70% in intensive care unit patients requiring renal replacement therapy, and more than 2 million people die from AKI each year. Currently available protein biomarkers for AKI do not permit diagnosis prior to significant loss of kidney function, and the most promising new diagnostic tests measure these biomarkers in both urine and serum. The aims of this study are to metabolically profile both urine and serum for biomarkers that allow for earlier detection of AKI and examine the effects of hypoxia-induced AKI on the structure of the kidney in mouse models.en_US
dc.titleIdentification of Urine Metabolic Biomarkers for Hypoxia-Induced Acute Kidney Injury Mouse Modelen_US
dc.typePosteren_US
dc.contributor.affiliationUndergraduate Research Forum
dc.contributor.affiliationChemistry Capstone CHM 492
dc.contributor.affiliationBiochemistry
dc.contributor.affiliationPre-medical Studies
dc.date.published2017


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