论文部分内容阅读
目的 研究表明整合素连接激酶(integrin-linked kinase,ILK)在肾脏疾病的发生、发展中起着重要作用.该研究旨在探讨ILK与儿章紫癜性肾炎(HSPN)肾小球损害的关系.方法 188例HSPN患儿按照国际儿童肾脏病组织(ISKDC)关于HSPN肾脏病理分级分成5组,即≤Ⅱa级组、Ⅱb级组、Ⅲa级组、Ⅲb级组、≥Ⅳ级组.对照组为薄基膜肾病患儿.采用免疫组织化学方法检测对照组及HSPN患儿.肾小球ILK的表达,分析肾小球ILK表达与肾小球病理损害、尿蛋白排泄量之间的关系.结果 ①ILK在肾小球的表达:对照、≤Ⅱa级、Ⅱb级、Ⅲa级、Ⅲb级、≥Ⅳ级组6组患儿肾小球ILK的阳性表达面积分别为:(3.35±1.01)%、(4.88±1.13)%、(9.64±1.36)%、(11.27±1.68)%、(17.42±3.0)%、(20.62±2.32)%,6组间比较,差异有非常显著性(P<0.01).②随着患儿尿蛋白排泄量的增加,肾小球ILK表达逐渐增强,尿蛋白阴性组、尿微量白蛋白组、显著尿蛋自组及大量尿蛋白组间的ILK表达差异有非常显著性(P<0.01).结论 ILK与儿童HSPN肾小球病理损害及蛋白尿的发生密切相关.“,”Objective Recent studies have shown that integrin-linked kinase (ILK) plays an important role in the pathogenesis and development of some kidney diseases. This study aimed to investigate the relationship between ILK and renal glomerular damage in children with Henoch-schonlein purpura nephritis ( HSPN). Methods One hundred and eighty-eight HSPN children (aged 3 to 17 years) were assigned to five groups according to the classification of the International Study of Kidney Disease in Children (ISKDC): grade ≤IIa (n =62), grade IIb(n =42) , grade IIIa(n = 29), grade IIIb(n =40) and grade≥IV(n = 15). Fifteen children with basement membrane nephropathy served as the control group. ILK expression on glomeruli was ascertained by immunohistochemical staining. The relationships of ILK expression on glomeruli with glomerular histopathologic lesions and urinary protein excretions were examined. Results The positive areas of ILK expression on glomeruli in the control, grade≤IIa, grade IIb, grade IIIa, grade IIIb and grade≥ IV groups were (3.35 ±1.01)%, (4. 88 ± 1. 13)% , (9. 64 ± 1. 36)% , (11. 27 ± 1. 68)% , (17.42±3.0)% and (20.62 ±2. 32% ) , respectively. There were significant differences in the ILK expression between groups (P < 0. 01). ILK expression on glomeruli increased with increased urinary protein excretions. There were significant differences in the ILK expression in children with different urinary protein excretions (P < 0. 01 ). Conclusions ILK might be involved in the process of renal glomerular histopathologic damage and the production of proteinuria in children with HSPN.