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dc.contributor.advisorYtrebø, Lars Marius
dc.contributor.authorMarkali, Pål Schmidt
dc.date.accessioned2015-09-10T08:54:52Z
dc.date.available2015-09-10T08:54:52Z
dc.date.issued2015-05-29
dc.description.abstractAcute kidney injury, formerly known as acute kidney failure, is a syndrome characterized by the rapid loss of the kidney´s excretory function. This is normally diagnosed by the accumulation of urea and creatinine, decreased urine output, or both. Acute kidney injury affects approximately 40% of critically ill patients and one third of them die within the first 90 days of admission. Despite the importance of this disease, no evidence-based treatment recommendations exists and the pathogenesis is debated. The concept of acute renal failure has undergone a modification the recent years. Traditionally acute renal failure has been related to ischemia and development of acute tubular necrosis. Mounting evidence suggests that acute, mild injury to the kidneys causes alterations to the urine output and blood chemistries. This could potentially have serious clinical consequences. The syndrome of acute kidney injury also includes patients without functional damage, but with impairment relative to physiologic demand. This means that AKI includes both injury and impairment. This is a more holistic approach to the clinical challenge, including patients that could benefit from early intervention. Sepsis is one of the main factors contributing to the development of acute kidney injury. Sepsis and septic shock account for approximately 50% of acute kidney injury cases in the ICU Though, the pathophysiology behind this development is inadequately understood. Systemic hypotension, renal vasoconstriction and ischemia-reperfusion injury as the mechanism behind septic acute kidney injury has been challenged. Septic acute kidney injury can occur during a hypo- and hyperdynamic circulatory state. It is associated with a high flow, low-pressure renal circulation. New histological findings indicate a lack of acute tubular necrosis and apoptosis during septic AKI, with only a minor influence of the tubular cells. Mounting evidence suggests exposure of the nephron and tubular cells to inflammatory mediators. This could alter the permeability of the glomerular filtration barrier through glycocalyx shedding, decreased fenestrae density and increased fenestrae diameter. Alterations to the permeability could possibly activate the tubuloglomerular feedback mechanism and result in a decrease in kidney function. Further research should focus on the intergrative glomerular barrier complex, with emphasis on glycocalyx, endothelial surface layer and fenestrae. New technology like PET and nanomechanics could be beneficial in the search for the pathogenesis behind septic AKI.en_US
dc.identifier.urihttp://hdl.handle.net/10037/8047
dc.identifier.urnURN:NBN:no-uit_munin_7628
dc.language.isoengen_US
dc.publisherUiT Norges arktiske universiteten_US
dc.publisherUiT The Arctic University of Norwayen_US
dc.rights.accessRightsopenAccess
dc.subject.courseIDMED-3950en_US
dc.subjectVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Nephrology, urology: 772en_US
dc.subjectVDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Nefrologi, urologi: 772en_US
dc.titleSeptic Acute Kidney Injuryen_US
dc.typeMaster thesisen_US
dc.typeMastergradsoppgaveen_US


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