FOR 1368: Hemodynamic Mechanisms of Acute Kidney Injury

该研究股由8个具有不同方法专长和长期合作历史的研究小组组成。急性肾损伤（AKI）包括一系列以肾小球滤过率突然下降为特征的综合征。多种原因可导致急性肾损伤，通常根据其来源分为肾内、肾前和肾后。导致急性肾损伤的损害范围从无明显形态特征的功能失调到肾小管破坏。在预防急性肾损伤或促进其解决的技术方面，已经作出了相当大的努力。不幸的是，在高危人群中预防AKI的发展是困难的。通过八组之间的真正合作和转化研究，我们追求以下目标：(1)确定区域循环的作用，特别是内通血管和外通血管，以及TRPV1在急性肾损伤病理生理中的作用；(2)阐明aki诱导的缺氧诱导因子（HIF）、细胞色素P450 （CYP）产物和NF-B的刺激机制；(3)建立有前景的急性肾损伤标志物及其来源；(4)制定预防或治疗局部缺血引起的急性肾损伤的新策略。总的来说，该研究单位旨在将急性肾损伤病理生理学的新见解转化为预防策略，以降低发病率和死亡率。

The Research Unit consists of eight research groups with different methodological expertise and a long-standing history of collaborations. Acute kidney injury (AKI) comprises a family of syndromes characterised by a sudden decrease in glomerular filtration rate. A multitude of causes may lead to acute kidney injury, which are commonly classified according to their origin as intrarenal, pre- and postrenal. The damage leading to acute kidney injury spans from functional dysregulation without overt morphological features to tubular destruction. Considerable effort has been made to develop techniques to prevent acute kidney injury or to facilitate its resolution. Unfortunately, preventing the development of AKI in at-risk populations is difficult. By true collaborative and translational research with interactions between the eight groups we pursue the following goals: (1) to define the role of regional circulation, particularly the vasa afferentia and vasa efferentia, and the role of TRPV1 in the pathophysiology of acute kidney injury; (2) to elucidate the mechanisms of AKI-induced stimulation of Hypoxia inducible factor (HIF), cytochrome P450 (CYP) products and NF-B; (3) to establish a promising marker for acute kidney injury and its origin; (4) to define a new strategy to prevent or treat acute kidney injury caused by local ischemia. As a whole, this Research Unit aims at transferring new insights from the pathophysiology of acute kidney injury into prevention strategies to reduce morbidity and mortality.