IgA肾病（IgAN）是世界范围内最常见的原发性肾小球疾病，其发病特点为循环IgA免疫复合物在肾脏的沉积，继而通过诱发一系列“瀑布式”炎症反应导致肾脏固有细胞的损伤。IgAN临床及病理表现形式多样，既往的研究提示血管内皮损伤在IgAN疾病进展及预后中扮演着重要角色,但是，何种因素参与IgAN血管内皮损伤，以及其机制如何，目前尚未完全明确。本人前期的研究发现IgAN患者升高的sFlt-1血浆水平参与IgAN血管损伤。那么,IgA免疫复合物是否可以通过诱导肾脏血管内皮细胞分泌过多sFlt-1，从而参与血管内皮损伤呢？本研究拟从体内试验中探索IgA免疫复合物-sFlt-1-内皮损伤的关系，并进一步在体外细胞刺激实验和IgAN动物模型上，阐明IgA免疫复合物通过诱导内皮细胞sFlt-1 表达参与IgAN血管内皮损伤的机制。本研究将对IgAN血管内皮损伤的机制做出补充，并为其防治提供新靶点和新思路。

IgA Nephropathy(IgAN) is the most common primary glomerulopathy in the world,characterized by the deposizion of IgA immune-complex in the kidney，which leads to the injury of renal inherent cells by inducing a series of inflammatary cascade . The clinical and pathological manifestation of IgAN is various, previous study suggested that vascular endothelial injury played important role in the disease progression and prognosis of IgAN, however,the factor participated in the vascular endothelial injury and the pathogenesis were still unknown. Our previous study proved elevated plasma sFlt-1 level was associated with the endothelial injury in patients with IgAN. Then, could IgA immune-complex induce the elevated expression of sFlt-1 in the endothelial cells and finally lead to endothelial injury? In this study, we will explore the relationship among IgA immune-complex, sFlt-1, as well as vascular endothelial injury in vivo, and furtherly clarify the pathogenesis of IgA immune-complex in the vascular endothelial injury of IgA Nephropathy by inducing the endothelial expression of sFlt-1 in vitro and IgAN animal model. Our study will give supplement regarding the pathogenesis of vascular endothelial injury in IgAN, and provide new target and new clue for the prevention and cure of the vascular endothelial injury in IgAN.