摘要
目的 研究人钠依赖二羧酸转运蛋白(human Na^+/dicarboxylate cotransporter,NaDC)在IgA肾病患者肾组织内表达的变化,探讨其在IgA肾病进展过程中的作用。方法 34例IgA肾病肾活检标本依据病理改变程度分为5级,同时对肾小管间质病变进行半定量分析。应用免疫组织化学技术观察肾组织内NaDC1和NaDC3的表达变化,并与临床指标进行相关分析。结果 随着IgA肾病病理改变程度的加重,肾小管间质病变亦加重。Ⅳ和Ⅴ级病变患者的24h尿蛋白定量、血肌酐和尿NAG酶均显著升高,尿渗透浓度显著下降(P<0.05)。NaDC1表达于近端肾小管上皮细胞的刷状缘上,与Ⅰ~Ⅲ级病例相比,Ⅳ和Ⅴ级病例中的NaDC1的表达减少,其中以Ⅴ级表达最少(P<0.05)。NaDC3表达于近端肾小管上皮细胞的基底侧膜上,与Ⅰ~Ⅱ级病例相比,Ⅱ~Ⅳ级病例中的NaDC3的表达增多,在Ⅴ级病例中,其表达显著减少(P<0.05)。肾小管NaDC1表达与尿NAG酶呈负相关(r=-0.627,P<0.05)。结论 钠依赖二羧酸转运蛋白的表达变化在IgA肾病进展过程中发挥重要的作用。
Objective To study the change of human Na+/dicarboxylate cotransporters (NaDC)in IgA nephropathy,and to discuss its role in IgA nephropathy. Methods Thirty-four cases of IgA nephropathy diagnosed by renal biopsy were divided into five grades according to the degree of pathological change of IgA nephropathy,and their tubulointerstitial lesions were semi-quantitatively analyzed. Changes of the expression of NaDC1 and NaDC3 in kidney were observed by using immunohistochemistry,and analyzed with clinical data by correlation. Results Tubulointerstitial lesion exacerbated with the progress of pathological change in IgA nephropathy. In the cases of Ⅳ and Ⅴ grade,24 h urinary protein,serum creatinine,urinary NAG enzyme were increased,and urinary osmotic pressure was decreased,as compared with the cases of Ⅰ-Ⅲ grade( P < 0. 05) . NaDCl expressed in brush border of proximal tubular cells,as compared with the cases of Ⅰ~ Ⅲ grade,its expression was decreased in the cases of IV and V grade and was the least in V grade ( P < 0. 05). NaDC3 expressed in basolateral membrane of proximal tubular cells,
as compared with the cases of Ⅰ-Ⅱ grade ,its expression was increased in the cases of Ⅲ and IV grade,but decreased significantly in Ⅴ grade (P<0.05).There was a negative correlation between the expression of NaDCl and urine NAG enzyme(r=-0. 627,P < 0. 05). Conclusion Na+/dicarboxylate cotransporters play important roles during the progress of IgA nephropathy.
出处
《中华肾脏病杂志》
CAS
CSCD
北大核心
2003年第5期297-300,共4页
Chinese Journal of Nephrology
基金
国家自然科学基金"创新研究群体科学基金"(30121005)
国家"十五"科技攻关计划(2001BA701A14a)
国家自然科学基金(30270505)