FOR 1368: Hemodynamic Mechanisms of Acute Kidney Injury

FOR 1368：急性肾损伤的血流动力学机制

• 批准号: 152203169
• 金额: --
• 依托单位: Institut für Vegetative Physiologie
• 依托单位国家: 德国
• 项目类别: Research Units
• 财政年份: 2011
• 资助国家: 德国
• 起止时间: 2010-12-31 至 2017-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/152203169?language=en
• 关键词: 1368; Hemodynamic; Mechanisms; Acute; Kidney

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.

研究股由八个研究小组组成，这些小组具有不同的方法专长和长期的合作历史。急性肾损伤（阿基）包括一系列以肾小球滤过率突然降低为特征的综合征。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包括从没有明显形态学特征的功能失调到肾小管破坏。已经做出了相当大的努力来开发预防急性肾损伤或促进其解决的技术。不幸的是，在高危人群中预防阿基的发展是困难的。通过八个小组之间相互作用的真正协作和转化研究，我们追求以下目标：（1）定义局部循环的作用，特别是血管传入和血管传出，以及TRPV 1在急性肾损伤病理生理学中的作用;（2）阐明AKI刺激缺氧诱导因子（HIF）、细胞色素P450（CYP）产物和NF-B的机制;（3）建立急性肾损伤及其起源的标志物;（4）确定预防或治疗局部缺血引起的急性肾损伤的新策略。作为一个整体，这个研究单位的目的是转移新的见解从急性肾损伤的病理生理学到预防策略，以减少发病率和死亡率。