血清25-羟基维生素D3水平与儿童糖尿病肾病的相关性研究

目的了解儿童糖尿病肾病患者血清维生素D的变化,并探讨维生素D对儿童糖尿病肾病发展的影响。方法 2015年6月—2018年2月从安阳地区医院共筛选69例儿童作为研究对象,分为1型糖尿病肾病组、2型糖尿病组和对照组,采用酶联免疫法测定25-羟基维生素D3[25(OH)D3]、甲状旁腺激素(PTH),采用免疫化学发光测定胰岛素(FINS)、C-肽(C-P)以及尿素氮(BUN)、肌酐(Scr)、尿微量白蛋白/肌酐比(ACR)。以25(OH)D3为因变量,分别以PTH、Ca、P、空腹血糖(FPG)、FINS、C-P、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、ACR为自变量,进行Pearson相关分析。结果各组资料对象的性别、年龄差异无统计学意义;与对照组比较,1型糖尿病肾病组、2型糖尿病组FPG、FINS、C-P、ACR和25(OH)D3差异均有统计学意义(P0.05)。25(OH)D3与FPG、ACR呈负相关,与FINS、C-P、Scr、BUN呈正相关(P0.05)。结论维生素D的减少促使儿童糖尿病的发生,参与了糖尿病肾病的发展,可能在1型糖尿病肾病的发病过程中起着重要作用。

Correlation between serum 25-hydroxyvitamin D3 levels and pediatric diabetic nephropathy

Objective To study the changes of serum vitamin D levels in children with diabetic nephropathy, and explore the effect of vitamin D on the development of children with diabetic nephropathy. Methods Children (69 cases) in Anyang District Hospital from June 2016 to February 2018 were divided into type 1 diabetic nephropathy group, type 2 diabetes group, and control group. 25-Hydroxyvitamin D3[25(OH) D3] and parathyroid hormone (PTH) were determined by enzyme-linked immunoassay, and insulin (FINS), C-peptide (C-P), urea nitrogen (BUN), creatinine (Scr) and urinary microalbumin/creatinine ratio (ACR) were determined by immunochemilu-minometric assay. 25(OH) D3 was taken as the dependent variable, and PTH, CA, P, FPG, FINS, C-P, TC, TG, HDL-C, LDL-C, and ACR as the independent variables, and Pearson correlation analysis was carried out. Results The sex and age of children in three groups were no difference. Compared with the control group, there were significantly different in FPG, FINS, C-P, ACR, and 25 (OH) D3 in type 1 diabetic nephropathy group and type 2 diabetic group (P<0.05). 25(OH) D3 was negatively correlated with FPG and ACR, and positively correlated with FINS, C-P, SCR and Bun (P<0.05). Conclusion The decrease of vitamin D promotes the occurrence of diabetes in children''s, participates the development of children with diabetic nephropathy, and vitamin D may play an important role in the pathogenesis of type 1 diabetic nephropathy.