复方血栓通胶囊对糖尿病肾病的疗效观察

目的 观察复方血栓通胶囊对减少糖尿病肾病(DN)患者尿微量白蛋白的疗效.方法 84例2型糖尿病患者患者进行12周降糖降压调脂等基础治疗后,按尿微量白蛋白/肌酐比值(ACR)水平分为正常白蛋白尿组(NAU)、低值白蛋白尿(LAU)、高值白蛋白尿组(HAU)、极高值白蛋白尿组(VHAU)4组,采用自身对照方法进行研究.在原治疗基础上加服复方血栓通胶囊每次3粒,每天3次,连用12周.观察治疗前后尿ACR、肝肾功能及血脂指标的变化.结果 LAU组及HAU组治疗后尿ACR显著降低(P＜0.01):治疗前肝肾功能或血脂异常的患者在治疗后相关指标明显改善(P＜0.05);治疗前肝肾功能或血脂正常的患者在治疗后相关指标无明显改变(P＞0.05).结论 复方血栓通胶囊有一定的降低早中期DN患者的尿ACR、改善肝肾功能和调节脂质代谢的作用.     

肾小球滤过率联合尿微量白蛋白与肌酐比值诊断糖尿病肾病的临床意义

目的:探讨2型糖尿病病人采用改良的中国公式计算肾小球率过滤(c-aGFR)联合尿微量白蛋白与尿肌酐比值(ACR)在诊断糖尿病肾病不同阶段中的临床意义,并做c-aGFR和ACR的相关性分析.方法:根据ACR不同阶段分成4组,A组(正常对照组),B组(糖尿病正常白蛋白尿组ACR＜ 30mg/g),C组(糖尿病肾病微量白蛋白尿组ACR30～300mg/g),D组(糖尿病肾病大量蛋白尿组ACR＞ 300mg/g);应用改良中国MDRD公式c-aGFR(mL/min·1.73m2)=175×[Hit Pcr]-1.234×年龄-0.179×[女性×0.79]计算GFR,(即c-aGFR,mL/min·1.73m2).双变量相关性分析采用Pearson相关分析.结果:与正常对照组相比糖尿病正常白蛋白尿组c-aGFR无明显变化(P＞0.05),糖尿病肾病微量白蛋白尿组与正常对照组相比c-aGFR降低,有显著变化(P＜0.05),糖尿病肾病大量蛋白尿组与正常对照组相比c-aGFR降低,有显著变化(P＜0.05),糖尿病肾病大量白蛋白尿组与糖尿病肾病微量蛋白尿组相比c-aGFR降低,有显著变化(P＜0.05).与正常对照组相比糖尿病正常白蛋白尿组ACR无明显变化(P＞0.05),糖尿病肾病微量白蛋白尿组与正常对照组相比ACR增高,有显著变化(P＜0.05),糖尿病肾病大量蛋白尿组与正常对照组相比ACR增高,有显著变化(P＜0.05),糖尿病肾病大量白蛋白尿组与糖尿病肾病微量蛋白尿组相比ACR增高,有显著变化(P＜0.05).c-aGFR随着ACR的增加呈下降趋势,Pearson分析显示二者具有显著负相关性.结论:c-aGFR及ACR可以做为糖尿病肾病诊断的重要监测指标;二者联合检测可以更准确的评估糖尿病患者肾脏功能的情况,对调整糖尿病患者经肾脏代谢的药物剂量及药物的选择都有极为重要的临床指导价值.     

Ⅱ型糖尿病合并肾病患者血压特点的观察

目的分析Ⅱ型糖尿病合并肾病(DN)患者的血压的特点。方法44例糖尿病肾病微量蛋白尿者(MAU),30例糖尿病肾病临床蛋白尿者(CAU),与96例糖尿病肾病合并高血压无蛋白尿者(NAU)相比较。结果随着尿蛋白排泄率(UAER)的增加,糖尿病病程、收缩压、脉压、甘油三脂逐渐升高。MAU组、CAU组与NAU组比较,无论入院时还是出院时使用的降压药的种数均增加。结论DN患者的高血压特点以收缩压和脉压升高为主,随着尿蛋白的增加,血压较难控制,使用降压药物种类增多。     

2型糖尿病肾病相关危险因素分析

目的 探讨2型糖尿病患者糖尿病肾病(DN)相关危险因素。方法 对258例2型糖尿病患者根据尿微量白蛋白/肌酐值(ACR)分为3组,分别是正常白蛋白尿组、微量白蛋白尿组、大量白蛋白尿组,同时对3组采集的数据进行统计分析。结果 大量白蛋白尿组和微量白蛋白尿组的糖尿病病程、糖化血红蛋白(HBA1C)、血尿酸(UA)、同型半胱氨酸(Hcy)、超敏C反应蛋白(CRP)高于正常白蛋白尿组,差异有统计学意义(P<0.05);logisitic回归分析中糖尿病病程和糖化血红蛋白被纳入回归方程,是糖尿病肾病的独立危险因素。结论 2型糖尿病病程长、血糖控制欠佳是糖尿病肾病发生发展的关键因素。血尿酸、同型半胱氨酸及C反应蛋白与糖尿病肾病具有相关性。     

血尿酸水平对2型糖尿病患者早期肾脏损害的影响

目的探讨血尿酸升高对2型糖尿病早期肾病的影响。方法根据血尿酸水平将2型糖尿病患者分成正常尿酸(NUA)组68例和高血尿酸(HUA)组52例,测定空腹血糖(FBG)、糖化血红蛋白(HbA1c)、血尿β2微球蛋白(β2-MG)、尿微量白蛋白(MAU)、尿N-乙酰-B-D-氨基葡萄糖苷酶(NAG)及尿肌酐,计算尿白蛋白尿肌酐比(ACR)及体重指数(BMI),进行统计学分析。结果 HUA组患者的尿NAG、ACR及血尿β2-MG均较NUA组升高,差异有统计学意义(P<0.05)。血尿酸水平与尿ACR、NAG及血尿β2-MG均呈正相关。结论血尿酸升高可加重2型糖尿病患者的早期肾损伤。     

血清TGF-β1水平与糖尿病肾病相关性研究

目的探讨糖尿病(DM)患者血清转化生长因子-β1(TGF-β1)含量及其与糖尿病肾病(DN)的关系。方法91例2型糖尿病患者根据尿白蛋白肌酐比值(ACR)分为单纯糖尿病组(A组)，微量白蛋白尿组(B组)和大量白蛋白尿组(C组)。采用ELISA双抗夹心法检测各组血清TGF-β1。含量，并采用免疫比浊法检测尿微量白蛋白(Alb)、转铁蛋白(TRF)、α1^-微球蛋白(α1^-MG)，同时检测各组尿肌酐(尿Cr)、空腹血糖(FPG)、糖基化血红蛋白(HbAlC)等。结果血清TGF-β1在3组之间有显著差异，尿TRF／Cr、α1^-MG／Cr、ACR经对教转化后3组之间亦有显著性差异，且其均随糖尿病肾病进程相平行升高。相关分析显示，血清TGF-β1与尿TRF／Cr，尿α1^-MG／Cr，ACR、FPG、HbAlC成正相关。结论TGF-β1。可能参与了糖尿病肾病的发生发展，测定DM患者血清TGF-β1。含量的变化，对于DN发病机制的研究，尤其是监测早期DN的发生和病情发展程度均有重要的价值。     

糖尿病肾病患者血清中miR-21表达及作用机制

目的：探讨糖尿病肾病患者血清中miR-21表达及作用机制。方法：选取2017-02～2019-03在我院治疗的糖尿病肾病患者350例,根据尿白蛋白/肌酐(UACR)水平分为：正常白蛋白尿组151例,微量白蛋白尿组126例,临床蛋白尿组73例,同时选取健康志愿者80例作为对照组。采用RT-PCR检测血清miR-21表达;选取HMC细胞,随机分为空白对照组、阴性转染组和miR-21mimics组,其中阴性转染组和miR-21 mimics组分别转染脂质体、miR-21 mimics,采用RT-PCR检测miR-21表达,Western blot检测Smad7和E-cadherin蛋白表达。结果：临床蛋白尿组血清miR-21相对表达量为(0.313±0.103),明显低于对照组、正常白蛋白尿组和微量白蛋白尿组(P<0.05);miR-21与UACR呈负相关(r=-0.537,P<0.05);miR-21 mimics组miR-21相对表达量为(1.102±0.122),明显高于空白对照组和阴性转染组(P<0.05);miR-21 mimics组Smad7和E-cadheri...     

2型糖尿病肾病患者外周血IGF-1、TGF-β和VEGF水平及临床意义

目的 探讨2型糖尿病肾病患者外周血胰岛素样生长因子-1(IGF-1)、转化生长因子-β(TGF-β)和血管内皮生长因子(VEGF)水平及临床意义.方法 选取2014年10月-2016年5月收治的100例2型糖尿病肾病患者,根据24 h尿白蛋白排泄量分为正常白蛋白尿组34例、微白蛋白尿组32例、高白蛋白尿组34例,另选32例正常健康体检者作为对照组.采集研究对象外周血及尿样,对IGF-1、TGF-β和VEGF水平及其他临床指标进行检测分析.结果 2型糖尿病肾病患者肌酐、尿素氮和收缩压随尿蛋白增高而增高(P＜0.05).高白蛋白尿组IGF-1水平高于对照组、正常白蛋白尿组和微白蛋白尿组(P＜0.05);正常白蛋白尿组、微白蛋白尿组和高白蛋白尿组TGF-β和VEGF水平均高于对照组(P＜0.01),高白蛋白尿组TGF-β水平高于正常白蛋白尿组和微白蛋白尿组(P＜0.05),高白蛋白尿组和微白蛋白尿组VEGF水平高于正常白蛋白尿组(P＜0.05).结论 检测IGF-1、TGF-β和VEGF水平能有效评估2型糖尿病肾病患者肾脏损伤程度,指导临床及时进行相关治疗.     

糖尿病患者尿微量蛋白检测的临床意义

目的 探讨非胰岛素依赖型糖尿病(NIDDM)患者尿微量蛋白的改变对糖尿病肾病(DN)早期诊断的临床意义。方法 应用免疫散射比浊法对86例非胰岛素依赖型糖尿病(NIDDM)患者进行尿微量蛋白的检测,并与正常对照组比较。结果 正常白蛋白尿组尿TRF较正常对照组明显升高,尿IGG、A1M无明显升高,微量白蛋白尿组尿IGG、IGG、AIM均明显升高,大量白蛋白尿组升高更为显著。结论 尿微量蛋白检测作为诊断糖尿病不同程度早期肾损害具有重要的临床意义。     

2型糖尿病白蛋白尿与颈动脉内膜中层厚度关系的探讨

目的:探讨2型糖尿病(T2DM)患者白蛋白尿与颈动脉内膜中层厚度的关系.方法:146例T2DM患者行24h尿微量白蛋白检测,根据结果分为正常白蛋白尿组(86例)和异常白蛋白尿组(60例,包括微量白蛋白尿组和大量白蛋白尿组),对2组患者分别进行各项生化指标及颈动脉内膜中层厚度(IMT)的检测,并对2组数据进行单因素、多因素Logistic回归分析,比较正常尿、微量白蛋白尿(MAU)以及大量白蛋白尿3组间颈动脉IMT的差异.结果:病程、视网膜病变发生率、三酰甘油、颈动脉IMT和血肌酐是2型糖尿病白蛋白尿的影响因素;病程长、三酰甘油高、颈动脉IMT增厚、血肌酐增高是2型糖尿病患者白蛋白尿的独立危险因素(OR值分别为1.105、1.528、12.781和1.029).3组间颈动脉IMT比较差异有统计学意义(P＜0.01),而微量白蛋白尿组与大量白蛋白尿组之间比较差异无统计学意义(P＞0.05).结论:2型糖尿病患者颈动脉IMT是白蛋白尿的一个独立危险因素,糖尿病肾病的严重程度增加,颈动脉IMT无明显增厚.     

糖尿病动脉粥样硬化与糖尿病肾病的关系

目的 探讨糖尿病动脉粥样硬化对糖尿病肾病患病率的影响.方法 根据颈动脉及下肢动脉超声检查结果,696例2型糖尿病(T2DM)患者分为T2DM伴动脉粥样硬化组(A组,551例)和T2DM无动脉粥样硬化组(B组,145例),测定两组肾小球滤过率(GFR)、24-h尿微量白蛋白.结果 两组24-h尿微量白蛋白和GFR相仿(P＞0.05).A组与B组的微量白蛋白尿和大量白蛋白尿患病率差异亦无统计学意义(22.7％和6.9％ vs.20.0％和3.4％)(P＞0.05).结论 糖尿病动脉粥样硬化不增加糖尿病肾病的发生.     

Characteristics of diabetic osteopenia in KK-Ay diabetic mice

We examined the bone mineral density (BMD) of the proximal region and the mid-diaphysis of the femur using dual energy X-ray absorption (DXA), the blood osteocalcin level and the blood glucose level every five weeks from 8 to 23 weeks old in KK-Ay diabetic mice. The BMD of the proximal region after 18 weeks old was significantly lower when compared with that at 8 weeks old (p<0.05), whereas there was no significant difference in the BMD of the mid-diaphysis at each week. The BMD of the proximal region at 18 weeks old was significantly lower than that in ddY mice, used as controls (p<0.05). The blood osteocalcin level at 18 weeks old was significantly lower than that at 8 weeks old and that in 18-week-old ddY mice (p<0.05). There was significant negative correlation between the blood glucose level and the BMD of the proximal region (r=-0.64, p<0.05). These results suggest that type 2 diabetes exerts an influence only on spongy bone, not on cortical bone, and that the BMD in the proximal region of the femur seems to be affected by blood glucose level, parallel with the progression of diabetes, through the blood osteocalcin level. In the present study, we show the characteristics of diabetic osteopenia in KK-Ay mice, an animal model of type 2 diabetes.     

Anti diabetic effect of cherries in alloxan induced diabetic rats

Diabetes mellitus (DM) is a metabolic disorder in the endocrine system resulting from a defect in insulin secretion, insulin action or both of them. Adverse side effects of chemical drugs for treatment of diabetes persuaded the using of medical plants. Cherry as a traditionally used plant for treatment of diabetes, is packed with powerful plant pigments called anthocyanins. They give cherries their dark red color and are one of the richest antioxidant sources which lower the blood sugar and bear other beneficial health effects. The purpose of this study is to evaluate the effect of ethanolic extract of cherry fruit on alloxan induced diabetic rats. In this study 36 Male Wistar rats, body weight of 150-200gr were divided into 6 groups. Diabetes was induced by intra peritoneal injection of 120 mg/kg Alloxan. The duration of the cherries treatment was 30 days in which single dose of extracts (200mg/kg) were oral administered to diabetic rats. Blood glucose levels were estimated with glucometer before treatment, 2h and 1- 4 weeks after administration of extracts. Treatment with extracts of the cherries resulted in a significant reduction in blood glucose and urinary microalbumin and an increase in the creatinine secretion level in urea. Extract of this plant is useful in controlling the blood glucose level. Cherries appear to aid in diabetes control and diminution of the complications of the disease. Some relevant patents are also outlined in this article.     

2型糖尿病患者蛋白尿与糖尿病视网膜病变的关系

目的 探讨2型糖尿病(T2DM)患者尿白蛋白/肌酐比值(UACR)与糖尿病视网膜病变(DR)的关系.方法 152例T2DM患者根据UACR均分为UACR正常(A)组(UACR＜30 mg/g)和UACR异常(B)组(UACR≥30 mg/g),根据糖尿病病程再分为病程＜10年(C)组(87例)和病程≥10年(D)组(65例).检测血糖、糖化血红蛋白,计算UACR.结果 B组DR患病率53.9％,明显高于A组的28.9％ (P＜0.05),B组发生DR的危险是A组的2.875倍(95％可信区间为1.471-5.620).C组中,UACR异常患者的DR患病率51.6％,明显高于UACR正常者的26.8％(P＜0.05),且前者发生DR的危险是后者的2.916倍(95％可信区间为1.162-7.314).结论 病程较短且UACR异常的T2DM患者发生DR的风险较高.     

糖尿病肌病综述

葡萄糖是细胞生长的重要调节因子,骨骼肌是全身利用葡萄糖的重要组织之一。研究表明葡萄糖灌注后约75%的糖被骨骼肌摄取,骨骼肌既是胰岛素作用的重要靶组织,也是胰岛素抵抗的主要部位[1,2]。当机体血糖升高时,骨骼肌的各种类型细胞及基质均可受损,因此骨骼肌成为糖尿病损害的主要靶器官之一,同时肌     

Predictors of diabetic nephropathy

Diabetic nephropathy (DN) is a leading cause of morbidity and mortality in diabetic patients representing a huge health and economic burden. Alarming recent data described diabetes as an unprecedented worldwide epidemic, with a prevalence of ～6.4% of the world population in 2010, while the prevalence of CKD among diabetics was approximately 40%. With a clinical field hungry for novel markers predicting DN, several clinical and laboratory markers were identified lately with the promise of reliable DN prediction. Among those are age, gender, hypertension, smoking, sex hormones and anemia. In addition, eccentric left ventricular geometric patterns, detected by echocardiography, and renal hypertrophy, revealed by ultrasonography, are promising new markers predicting DN development. Serum and urinary markers are still invaluable elements, including serum uric acid, microalbuminuria, macroalbuminuria, urinary liver-type fatty acid-binding protein (u-LFABP), and urinary nephrin. Moreover, studies have illustrated a tight relationship between obstructive sleep apnea and the development of DN. The purpose of this review is to present the latest advances in identifying promising predictors to DN, which will help guide the future research questions in this field. Aiming at limiting this paramount threat, further efforts are necessary to identify and control independent modifiable risk factors, while developing an integrative algorithm for utilization in DN future screening programs.     

Management of diabetic ketoacidosis

Diabetic ketoacidosis is an all too frequent and sometimes preventable complication of Type I diabetes mellitus, responsible for significant morbidity and mortality within the diabetic population. Precipitating diseases account for the majority of deaths occurring in patients admitted in diabetic ketoacidosis, but some deaths are still attributable to ketoacidosis alone, despite recent advances in therapy and management. Recognition of the ketoacidotic state is paramount to optimal therapy, and often hinges on the diagnostic acumen of the physician. Since 20 to 30% of patients presenting in diabetic ketoacidosis do so as the initial manifestation of their previously undiagnosed disease, physicians must maintain a high level of suspicion for this condition. Understanding the pathogenetic mechanisms leading to and prevailing in diabetic ketoacidosis will allow physicians to intervene in a rational manner, approaching therapy with specific end-points in mind: (a) restoration of optimal volume status; (b) reversal of acidosis; (c) reduction of serum glucose levels; (d) replacement of specific electrolytes in a timely manner; (c) institution of appropriate therapy for any precipitating cause; and, (f) careful monitoring of the patient's biochemical, physical and mental parameters to allow adjustment in therapy as necessary. The mainstay of treatment for diabetic ketoacidosis is appropriate fluid and insulin therapy. Low-dose intravenous infusion is now the accepted mode of insulin delivery for patients with this condition. Potassium replacement is almost always necessary, often requiring massive amounts of this ion due to the total body depletion seen with the development of ketoacidosis. Controversy still surrounds routine use of phosphate in diabetic ketoacidosis but replacement may be needed if serum levels fall toward the lower limits of normal values, to avoid the potential adverse effects of phosphate depletion. Administration of bicarbonate is also controversial and should be reserved for patients whose pH is less than 7.0 to 7.1 and then it should be added to intravenous fluids, not given as an intravenous bolus. Efforts toward preventing diabetic ketoacidosis should be of prime importance to physician and patient alike. Preventive measures should include patient education about diabetes mellitus, precipitating factors of diabetic ketoacidosis, signs and symptoms of early metabolic decompensation, rational insulin therapy during minor illness and appropriate timing of physician contact to help avoid this serious and sometimes fatal complication of diabetes mellitus.