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作 者:曾雪琪[1] 许自川[1] 党西强[1] 何小解[1] 易著文[1]
机构地区:[1]中南大学湘雅二医院小儿肾脏病研究室,湖南省小儿肾脏病临床中心,湖南长沙410011
出 处:《中国当代儿科杂志》2009年第9期717-721,共5页Chinese Journal of Contemporary Pediatrics
基 金:国家自然科学基金(30500546);湖南省科技厅科技计划项目(06SK-3029-11)
摘 要:目的探讨小儿紫癜性肾炎(HSPN)肾组织血管内皮生长因子(VEGF)表达与肾脏病理、肾间质微血管损伤的关系。方法选取32名该院确诊的HSPN患儿为观察组,均符合中华医学会儿科学分会肾脏病学组修订的诊断标准,入院前未应用激素及其他免疫抑制剂,5例因肾外伤切除肾组织患者为对照组。所有肾脏标本进行常规苏木精-伊红染色,并进行微血管评分。免疫组化法检测VEGF及CD34的表达,以CD34作为微血管内皮细胞标志。计数微血管密度(MVD),分析肾脏VEGF表达与肾脏病理积分、微血管积分之间的关系。结果①与对照组和病理分级Ⅱ级HSPN组相比,病理分级Ⅲ级及以上HSPN患儿肾脏微血管密度明显减低,并随病理分级的增加而减少,各组之间差异存在显著性。②与对照组相比,Ⅱ级HSPN组肾脏微血管评分无明显变化,Ⅲa、Ⅲb级、Ⅳ、Ⅴ级组肾脏微血管评分明显降低,随着病理分级的加重,肾脏微血管评分逐渐降低,各级之间差异有显著性(P<0.05)。③与对照组相比,VEGF表达在病理分级Ⅱ级组表达较对照组升高(P<0.05),而Ⅳ/Ⅴ级组则较对照组降低(P<0.05),Ⅲa级、Ⅲb级组与对照组比较差异无显著性。HSPN组随着肾脏病理改变的加重,VEGF表达逐渐下降,各级之间比较差异有显著性(P<0.05)。④Spearman相关性分析结果显示,肾组织VEGF表达与微血管密度变化一致,二者呈正相关,相关系数为0.953,P<0.01。结论VEGF表达减低可能参与了HSPN肾脏病理损害及微血管损害。Objective To investigate the relationship between vascular endothelial growth factor (VEGF) expression and microvessel injury of renal interstitium in children with Henoch-Schonlein purpura nephritis ( HSPN ). Methods Thirty-two children with HSPN and who had not received glucoeorticoid or immunodepressants treatment before hospitalization were enrolled. Five children undergoing nephrectomy due to renal trauma were used as the control group. Renal samples were stained by hematoxyfin and eosin and renal pathological changes were evaluated semi-quantitatively. CD34 and VEGF expression was detected by immunohistochemistry. CD34 was used as the marker for endothelial cells of renal microvessels. The microvessel density (MVD) was calculated by CD34 immunostaining. Results Compared with the control and the renal pathological grade Ⅱ HSPN groups, MVD in the grade Ⅲ and above HSPN groups decreased significantly, with an obvious reduction in MVD with the increased renal pathological grade ( P 〈 0.05 ). The renal microvessel score in the grades Ⅲa, Ⅲb, Ⅳ, and Ⅴ HSPN groups decreased obviously compared with that in the control group. The renal microvessel score decreased with the increased renal pathological grade ( P 〈 0.05 ). VEGF expression in the grade Ⅱ HSPN group was higher ( P 〈 0. 05 ), while that in the grades IV and V HSPN group was lower than that in the control group (P 〈 0.05 ). VEGF expression in the HSPN group showed a significant reduction with the increased renal pathological grade ( P 〈 0.05 ). There was a positive correlation between VEGF expression and MVD in renal tissue in the HSPN group ( r = 0. 935, P 〈 0.01 ). Conclusions The decreased expression of VEGF may be responsible for the renal pathological damage and microvessel injury in HSPN.
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