{"title":"Expression of response gene to complement-32 in renal tissue of children with immunoglobulin A nephropathy.","authors":"Xiao-Ling Niu, Xin-Yu Kuang, Zhi-Gang Zhang, Xue-Guang Liu, Zhong-Hua Zhao, Xin Zhang, Hong Xu, Wen-Yan Huang","doi":"10.3109/00365599.2011.585624","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the expression and significance of response gene to complement-32 (RGC-32) in renal tissue of children with immunoglobulin A nephropathy (IgAN).</p><p><strong>Material and methods: </strong>Forty-five patients diagnosed as having IgAN by renal biopsy were enrolled. The expression of RGC-32, α-smooth muscle actin (α-SMA) and transforming growth factor-β(1) (TGF-β(1)) was observed by immunohistostaining. The relationshis between the expression of RGC-32, α-SMA, TGF-β1, degree of renal pathological lesions in IgAN and clinical index were assessed by Spearman correlation.</p><p><strong>Results: </strong>Immunohistostaining analysis showed that RGC-32 protein was present in epithelial cells of renal tubules in normal and IgAN renal tissues. With more severe renal pathological lesions, the expression of RGC-32 in IgAN was increased. The expression of RGC-32 was positively correlated with that of α-SMA, TGF-β(1) and the degree of renal pathological lesions in children with IgAN (p < 0.05), but had no relationship with serum creatinine, urinary N-acetyl-β-d-glucosaminidase/creatinine, urinary microalbuminuria/creatinine, urinary microimmunoglobulin/creatinine or urinary α(1)-microglobulin/creatinine ratio (p > 0.05).</p><p><strong>Conclusion: </strong>Expression of RGC-32 can reflect the degree of renal pathological lesions in IgAN. RGC-32 may participate in the renal tubulointerstitial lesions in children with IgAN, especially in epithelial -mesenchymal transition induced by TGF-β(1).</p>","PeriodicalId":21543,"journal":{"name":"Scandinavian Journal of Urology and Nephrology","volume":"45 5","pages":"371-6"},"PeriodicalIF":0.0000,"publicationDate":"2011-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/00365599.2011.585624","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Scandinavian Journal of Urology and Nephrology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/00365599.2011.585624","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2011/6/16 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 5
Abstract
Objective: This study aimed to investigate the expression and significance of response gene to complement-32 (RGC-32) in renal tissue of children with immunoglobulin A nephropathy (IgAN).
Material and methods: Forty-five patients diagnosed as having IgAN by renal biopsy were enrolled. The expression of RGC-32, α-smooth muscle actin (α-SMA) and transforming growth factor-β(1) (TGF-β(1)) was observed by immunohistostaining. The relationshis between the expression of RGC-32, α-SMA, TGF-β1, degree of renal pathological lesions in IgAN and clinical index were assessed by Spearman correlation.
Results: Immunohistostaining analysis showed that RGC-32 protein was present in epithelial cells of renal tubules in normal and IgAN renal tissues. With more severe renal pathological lesions, the expression of RGC-32 in IgAN was increased. The expression of RGC-32 was positively correlated with that of α-SMA, TGF-β(1) and the degree of renal pathological lesions in children with IgAN (p < 0.05), but had no relationship with serum creatinine, urinary N-acetyl-β-d-glucosaminidase/creatinine, urinary microalbuminuria/creatinine, urinary microimmunoglobulin/creatinine or urinary α(1)-microglobulin/creatinine ratio (p > 0.05).
Conclusion: Expression of RGC-32 can reflect the degree of renal pathological lesions in IgAN. RGC-32 may participate in the renal tubulointerstitial lesions in children with IgAN, especially in epithelial -mesenchymal transition induced by TGF-β(1).