蛋白尿是肾病恶化进展的独立危险因素，目前临床多以辨证论治为主，外治法挖掘及深入的机制研究尚不多见。"蛋白尿从络病论治"理论认为,肾络郁滞致病与肾小球滤过屏障（GFB）损伤及肾纤维化形成相关。血管内皮生长因子（VEGF）通过诱导血管内皮分化及多窗孔结构的形成维持GFB功能完整性；并通过抑制TGF-β1诱导肾小管上皮细胞-间充质转化（EMT）干预肾纤维化进程。据此提出假说，灸法活血通络调整肾络郁滞状态以改善肾小球滤过功能和抑制肾纤维化。本课题以局灶硬化性肾炎（FSGS）模型大鼠为研究对象，以科素亚作为对照，通过观察不同灸时灸法对FSGS模型大鼠肾脏病理组织结构变化及VEGF、VEGFR-2、TGF-β1、HGF、AngⅡ、ET、NO、α-SMA等因子表达的影响，从VEGF调节GFB、抑制EMT角度研究FSGS蛋白尿机制和艾灸的活血通络作用，以期为临床应用外治灸法治疗肾病蛋白尿提供部分理论依据

Proteinuria is an independent risk factor for progressive kidney disease.Currently，clinicians put more focus on TCM syndrome distribution. External treatment on proteinuria is seldom to take actively as well as its research on mechanism. there are many researches on the collateral disease theory to proteinuria. The major point of this view suggest that glomerular filtration barrier (GFB) injured and tubulointerstitial fibrosis due to the statement of blood stasis in collateral vessels of kidney.Vascular endothelial growth factor (VEGF) maintains GFB functional integrity by inducing vascular endothelial differentiation and multi- fenestrae structure formulation, and intervents to the progress of tubulointerstitial fibrosis by inhibiting TGF-β1-induced epithelial-myofibroblast transition(EMT). Above all, we suggest that moxibustion adjust the statement of blood stasis in collateral vessels of kidney by activating blood circulation and freed the collateral vessels, so as to improve the glomerular filtration rate and tubulointerstitial fibrosis.The study chooses FSGS rat models as the method to observe the influence of moxibustion in different time and methods to renal pathological changes in the structure and cytokines, such as VEGF,VEGFR-2,TGF-β1,HGF,AngⅡ,AT1R,ET,NO,α-SMA,FN and Col-I. We try to explain the mechanism of proteinuria on FSGS and the effect of moxibustion activating blood circulation and freed the collateral vessels which related to VEGF regulating GFB and inhibiting EMT, so as to privide a clinical theoretical basis of moxibustion intervention to proteinuria on kidney disease.