INFLAMMATORY BIOMARKERS & ACUTE RENAL FAILURE IN CARDIOPULMONARY BYPASS SURGERY

炎症生物标志物

• 批准号: 7718555
• 负责人: MITCHELL H ROSNER
• 金额: $ 5.26万
• 依托单位: UNIVERSITY OF VIRGINIA
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-03-01 至 2009-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7718555
• 关键词: Acute Kidney Failure; Acute Renal Failure with Renal Papillary Necrosis; Biological Markers; Bypass; Cardiac; Cardiopulmonary Bypass; Clinical; Computer Retrieval of Information on Scientific Projects Database; Creatinine; Diagnosis; Dipeptidyl-Peptidase IV; Event; Failure; Funding; Grant; Inflammatory; Injury; Institution; Insulin-Like Growth-Factor Binding Protein 1; Intensive Care Units; Interleukin-6; Intervention; Kidney; Methods; Operative Surgical Procedures; Patients; Research; Research Personnel; Resources; Serum; Source; Staging; Therapeutic Intervention; Tubular formation; United States National Institutes of Health; base; cytokine; mortality; novel; prevent; urinary

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Acute kidney injury (AKI) is associated with substantial mortality expecially when it occurs in the intensive care unit or post-cardiac bypass surgery. Thus far, all therapeutic interventions to either prevent or treat AKI have failed. In part this failure is due to late diagnosis of AKI. Typically, AKI is diagnosed based upon the rise in serum creatinine. When this occurs, however, substantial injury has already taken place and therapies are likely to be unsuccessful. There is great need for methods of diagnosis AKI at the very earliest stages when there is hope that interventions to protect the kidney may be successful. We aim to determine if a novel urinary biomarker of proximal tubular injury (adenosine deaminase binding protein-26) can detect clinical meaningful acute kidney injury before rises in serum creatinine are detectable. Furthermore, we aim to determine the temporal profile of pro-inflammatory cytokines (IL-1B, IL-6, and TNF-a) in patients undergoing cardiopulmonary bypass surgery and compare these profiles between patients developing acute kidney injury and those who do not develop kidney injury. Lastly, we aim to discover novel urinary biomarkers that can discriminate between AKI and rises in serum creatinine that are not associated with AKI. Ultimately, these biomarkers will be used to define the early events of AKI and allow for therapy at the earliest signs of renal injury.

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