INFLAMMATORY BIOMARKERS & ACUTE RENAL FAILURE IN CARDIOPULMONARY BYPASS SURGERY

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 急性肾损伤（阿基）与大量死亡率相关，特别是当它发生在重症监护病房或心脏搭桥手术后时。 到目前为止，所有预防或治疗阿基的治疗干预都失败了。 这种失败部分是由于阿基的诊断较晚。 通常，阿基的诊断基于血清肌酐的升高。 然而，当这种情况发生时，已经发生了实质性的损伤，并且治疗可能不成功。 非常需要在最早阶段诊断阿基的方法，此时有希望保护肾脏的干预措施可能会成功。 我们的目的是确定一种新的近端肾小管损伤的尿生物标志物（腺苷脱氨酶结合蛋白-26）是否可以在血清肌酐升高之前检测出具有临床意义的急性肾损伤。 此外，我们的目的是确定在接受心肺转流手术的患者中促炎细胞因子（IL-1B，IL-6和TNF-α）的时间分布，并比较发生急性肾损伤的患者和未发生肾损伤的患者之间的这些分布。 最后，我们的目标是发现新的尿液生物标志物，可以区分阿基和与阿基无关的血清肌酐升高。最终，这些生物标志物将用于定义阿基的早期事件，并允许在肾损伤的最早体征时进行治疗。

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.