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目的 :了解血管内皮细胞生长因子 (VEGF)及其受体 (VEGF R)在 2型糖尿病肾病患者肾组织中的变化及其与糖尿病肾病 (DN)临床与病理表现之间的关系。 方法 :以正常肾组织为对照 ,采用特异性抗体和免疫组织化学染色方法 ,对 3 0例DN患者肾组织中VEGF和VEGF R的分布及其强度变化进行了观察 ,并结合临床及肾脏病理进行了分析。 结果 :DN患者肾小球VEGF和VEGF R无论在分布上 ,还是在强度变化上与正常人相比均有明显差异。DN患者肾小球VEGF和VEGF R表达增加与患者蛋白尿 ( 83 3 %vs3 3 3 % ,P <0 0 1)、糖尿病视网膜病变 ( 66 7%vs 16 7% ,P <0 0 1)关系密切 ,而与高血压 ,糖化血红蛋白水平之间无明显相关性。DN患者肾小球VEGF和VEGF R表达增加还与肾小球内皮细胞损伤所致的一些组织形态学改变 ,如K W结节 ( 72 2 %vs 16 7% ,P<0 0 5 )、肾小球内皮细胞增生 ( 66 7%vs3 3 3 % ,P <0 0 5 )及微血管瘤形成 ( 61 6%vs 2 5 0 % ,P <0 0 5 )的发生显著相关。 结论 :DN患者肾组织中VEGF及VEGF R2的表达增加与DN患者的蛋白尿形成、糖尿病视网膜病变和内皮细胞损伤所致的形态学改变关系密切。VEGF介导了DN患者肾小球内皮细胞损伤和功能紊乱的发生。
Objective: To investigate the changes of vascular endothelial growth factor (VEGF) and its receptor (VEGFR) in renal tissue of patients with type 2 diabetic nephropathy and its relationship with the clinical and pathological manifestations of diabetic nephropathy (DN). Methods: The distribution and intensity of VEGF and VEGF R in renal tissue of 30 DN patients were observed by using specific antibody and immunohistochemical staining. The clinical and renal pathology Analysis. Results: There was a significant difference in the distribution of VEGF and VEGF R in glomerular of DN patients compared with normal subjects. Increased expression of VEGF and VEGF R in glomeruli of patients with DN correlated with proteinuria (83 3% vs 33 3%, P 0 01), diabetic retinopathy (66 7% vs 16 7%, P 0 01) Close, but not with high blood pressure, HbA1c level. Increased expression of VEGF and VEGF R in glomeruli of DN patients was also associated with some morphological changes caused by glomerular endothelial cell injury such as KW nodules (72.2% vs 16.7%, P <0.05) There was a significant correlation between the proliferation of endothelial cells (66 7% vs 33 3%, P 0 05) and microvessel angiogenesis (61 6% vs 25 0%, P 0 05). Conclusion: The increased expression of VEGF and VEGF R2 in renal tissue of DN patients is closely related to the formation of proteinuria, diabetic retinopathy and the morphological changes induced by endothelial cell injury in patients with DN. VEGF mediates glomerular endothelial cell injury and dysfunction in DN patients.