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出 处:《现代检验医学杂志》2017年第5期94-96,99,共4页Journal of Modern Laboratory Medicine
基 金:宁夏医科大学临床医学一流学科建设项目;2017年宁夏"研究生教育创新计划"学位点建设项目(YXW 2017014);宁夏高等学校科学研究重点项目(NGY2013058)~~
摘 要:目的研究尿α1-微球蛋白(α1-MG)和尿激肽原1(KNG1)水平在单纯性2型糖尿病与糖尿病肾病患者中的表达变化情况。方法选取2016年9月~2017年3月在宁夏医科大学总医院住院的糖尿病肾病患者34例作为实验组(DN组)以及同时期单纯性2型糖尿病患者32例作为对照组(DM组),其中,DN组包括甲组(HbA1c<10%)19例和乙组(HbA1c≥10%)15例。测定尿α1-MG和尿KNG1及各项生化指标。结果与DM组相比,尿α1-MG在DN组下降(t=9.972,P<0.01),尿KNG1在DN组升高(t=-3.356,P<0.01),差异均具有统计学意义;DN乙组尿α1-MG、血清GLU水平均高于DN甲组(t=-2.092,-3.464,均P<0.05),DN乙组血清Cr水平低于DN甲组,差异具有统计学意义(t=2.181,P<0.05);此外,在DN组,根据Pearson相关分析显示,尿α1-MG与HbA1c,尿KNG1呈正相关(r=0.33和0.355,均P<0.05),其它未见明显相关。结论尿α1-MG和KNG1的表达在DN的发生发展中存在一定的变化规律,可为DN的临床诊断提供依据。Objective To explore the changes of detection of urine α1-MG and KNG1 in simple type 2 diabetes mellitus and diabetic nephropathy patients. Methods 66 cases of diabetic patients in General Hospital of Ningxia Medical University from September 2016 to March 2017 were recruited,and the patients were divided into two groups, as follows., the diabetic ne- phropathy (DN) group 34 cases as experimental group,and the simple type 2 diabetes mellitus (DM) group 32 cases as control group. Than DN group was divided into two groups according to HbAIc,A groups 19 cases HbAlc was less than 10G, B groups 15 cases HbAlc was greater than or equal to 10%. The urine α1-MG,urine KNG1 and other biochemical indicators were mearured for all subjects. Results Compared with the DM group,the urine α1-MG in DN group was significantly lower (t=9. 972,P〈0.01),but the result of the urine KNG1 was the opposite (t=-3. 356,P〈0.01). The urine α1-MG and ser- um GLU in B group were significantly higher than those of the A group (t=-2. 092,-3. 464,all P〈0.05) ,but the result of the serum Cr was the opposite (t= 2. 181, P〈0.05). The level of urine α1-MG in DN group were positively correlated with HbAlc and urine KNG1 (r=0.33,0. 355,all P〈0.05). Conclusion There were some changes in the expression of urine α1-MG and KNG] in the occurrence and development of diabetic nephropathy, which provide the basis for the clinical di agnosis of diabetic nephropathy.
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