1例糖尿病肾病微量白蛋白尿期患者的循证治疗

目的为1例伴微量白蛋白尿的2型糖尿病患者制定治疗方案。方法根据患者临床特点,提出“对糖尿病肾病微量白蛋白尿期患者进行针对可能导致病情加重的多个危险因素的强化治疗是否能改善其预后”等5个临床问题,检索Cochrane图书馆(2005年4期),ACP Journal Club (1991～2005),MEDLINE(1991～2005),纳入糖尿病肾病治疗的系统评价、Meta分析、随机对照试验和临床指南,根据所获最佳临床证据为患者制定治疗方案。结果共纳入14个研究。现有证据显示,对糖尿病肾病微量白蛋白尿期患者进行针对可能导致病情加重的多个危险因素的强化治疗,包括严格控制血糖、血压,调脂,限制蛋白的摄入,戒烟等能延缓或阻止糖尿病肾病的进展。结论影响糖尿病患者病情加重的因素包括生活方式(饮食、运动、戒烟)、血糖、血压、血脂高低等,对其进行的干预,能有效缓解患者症状,提高患者长期生存质量。     

初诊2型糖尿病患者尿微量白蛋白的排泄率观察

目的：观察初诊2型糖尿病患者有无早期肾病，方法：观察住院165例2型糖尿病患者晨尿微量白蛋白，分初诊组，复诊组，对照组以t检验比较，结果：初诊2型糖尿病组有20％尿微量白蛋白增高，可能诊为早期肾病，但无临床肾病发现，糖尿病病程愈长，尿微量白蛋白愈高，直到临床肾病期，结论：初诊2型糖尿病实际病程已数年，尽早诊断糖尿病并干预治疗对糖尿病患者预防十分重要。     

诺和锐30治疗2型糖尿病肾病的临床分析

目的 探讨诺和锐30对不同分期2型糖尿病肾病的治疗效果.方法 63例2型糖尿病肾病患者按尿蛋白定性,分为尿蛋白阴性而尿微量白蛋白排泄率≥20μg/min的微量白蛋白尿组(A组)41例和尿蛋白阳性的蛋白尿组(P组)22例,根据血糖每日早晚2次餐前15分钟皮下注射诺和锐30.治疗16周后观察诺和锐30影响糖尿病肾病患者尿微量白蛋白排泄率情况.结果 与治疗前比较,治疗后A组和P组的尿微量白蛋白排泄率降低分别为(44.5±16.2)%和(28.9±23.6)%,两组比较差异有显著性 (P＞0.05).结论 诺和锐30对2型糖尿病肾病患者的尿微量白蛋白有明显改善.     

厄贝沙坦对2型糖尿病肾病微量白蛋白尿的治疗作用

目的观察厄贝沙坦合并常规治疗方法治疗2型糖尿病肾病微量白蛋白尿患者的效果。方法将我院80例2型糖尿病肾病微量白蛋白尿患者,随机平均分为两组,在常规降糖、抗凝、降脂、低蛋白饮食治疗的基础上,治疗组：加用厄贝沙坦;对照组：常规治疗未加厄贝沙坦。所有病例于治疗前及治疗3个月、6个月时抽血测定空服血糖（FBG）、餐后血糖（PBG）、内生肌酐清除率（Ccr）、血尿素氮（BUN）、24hUpro、UAER、ACR检测,然后对治疗前后两组分别进行对比分析。结果治疗组2型糖尿病肾病微量白蛋白尿患者,在常规降糖、抗凝、降脂、低蛋白饮食治疗的基础,上加用厄贝沙坦,治疗3个月、6个月后24hUpro、UAER、ACR明显要好于对照组。结论厄贝沙坦治疗2型糖尿病肾病微量白蛋白尿临床疗效显著可靠。     

运动锻炼对2型糖尿病肾病患者血压、脂蛋白（a）及尿微量白蛋白的影响

目的　研究运动锻炼对 2型糖尿病肾病 (DN)患者血压、脂蛋白 (a)及尿微量白蛋白的影响。方法　将 80例 2型DN患者随机分为治疗组与对照组 ,每组各 40例。对照组维持原糖尿病治疗方案不变 ,治疗组在原治疗方案的基础上进行运动锻炼 ,观察 8周。结果　治疗后 ,两组患者血压、尿微量白蛋白及脂蛋白 (a)均降低 (P <0 .0 5) ,治疗组明显优于对照组 (P <0 .0 1)。结论　适量运动锻炼对降低 2型DN患者的血压、脂蛋白 (a)及尿微量白蛋白具有积极的作用     

厄贝沙坦对2型糖尿病肾病微量白蛋白尿的治疗作用

目的 观察厄贝沙坦合并常规治疗方法治疗2型糖尿病肾病微量白蛋白尿患者的效果.方法 将我院80例2型糖尿病肾病微量白蛋白尿患者,随机平均分为两组,在常规降糖、抗凝、降脂、低蛋白饮食治疗的基础上,治疗组:加用厄贝沙坦;对照组:常规治疗未加厄贝沙坦.所有病例于治疗前及治疗3个月、6个月时抽血测定空服血糖(FBG)、餐后血糖(PBG)、内生肌酐清除率(Ccr)、血尿素氮(BUN)、24 h Upro、UAER、ACR检测,然后对治疗前后两组分别进行对比分析.结果 治疗组2型糖尿病肾病微量白蛋白尿患者,在常规降糖、抗凝、降脂、低蛋白饮食治疗的基础,上加用厄贝沙坦,治疗3个月、6个月后24 h Upro、UAER、ACR明显要好于对照组.结论 厄贝沙坦治疗2型糖尿病肾病微量白蛋白尿临床疗效显著可靠.     

缬沙坦治疗老年早期糖尿病肾病的疗效观察

目的观察缬沙坦对糖尿病肾病患者尿蛋白的影响,探讨应用该药物对早期糖尿病肾病的保护作用。方法37例2型糖尿病肾病患者,应用缬沙坦治疗12周,测定患者肾功能、血钾、血糖及24 h尿总蛋白、尿微量白蛋白含量。结果缬沙坦能明显降低2型糖尿病患者尿总蛋白及微量白蛋白的排泄率（〈0.01）。结论缬沙坦能够阻止或延缓早期糖尿病肾病的发展,适用于糖尿病肾病患者。     

尿液生物标记物在早期2型糖尿病肾病诊断中的价值探讨

目的检测2型糖尿病早期肾病患者的尿中性粒细胞明胶酶相关脂质运载蛋白(NGAL)和胱抑素-C的水平,并与无糖尿病肾病的患者进行比较,分析尿NGAL和胱抑素C水平与尿微量白蛋白相关性。方法入组126名2型糖尿病患者和30名无糖尿病肾病作为对照组进行横断面比较研究。分为3个研究组:2型糖尿病有微量白蛋白尿组,2型糖尿病无微量白蛋白尿组和无任何肾脏疾病的患者。统计研究对象中2型糖尿病病程时间和血糖状态。对所有受试者的血样集中储存在-20℃的冰箱中,批量检测尿微量白蛋白以及NGAL和胱抑素-C水平。结果微量白蛋白尿患者的尿NGAL和胱抑素-C水平(228.18和3.23ng/ml)与无蛋白尿(146.12和2.61ng/ml)和对照组(26.56和0.30ng/ml)相比显著升高。尿NGAL和胱抑素C水平与糖尿病患者微量白蛋白尿呈线性相关。结论尿NGAL和胱抑素C水平早期糖尿病肾病患者较无糖尿病肾病患者升高。尿NGAL和胱抑素-C水平与2型糖尿病患者微量白蛋白尿(尿白蛋白肌酐比值)呈正相关。     

2型糖尿病患者血浆同型半胱氨酸检测的临床意义

目的探讨同型半胱氨酸与2型糖尿病并发糖尿病肾病的关系。方法根据24h尿白蛋白排泄量将患者分为3组，单纯2型糖尿病组、微量白蛋白尿组、大量白蛋白尿组及正常对照组，分别检测其同型半胱氨酸、空腹血糖、糖化血红蛋白。结果糖尿病肾病患者血浆同型半胱氨酸高于正常健康人，并随病情的加重而升高，但单纯2型糖尿病患者血浆同型半胱氨酸与正常健康人相比未发现明显差异。结论高同型半胱氨酸与2型糖尿病肾病的发生、发展有关。     

银杏叶提取物治疗早期糖尿病肾病的Meta分析

目的采用Cochrane系统评价方法,评价银杏叶提取物治疗早期糖尿病肾病的疗效和安全性。方法检索Cochrane图书馆临床对照试验数据库(2013年第2期)、PubMed(1978²013年)、维普中文期刊数据库(19892013年)、维普中文期刊数据库(1989²013年)、中国期刊全文数据库(19792013年)、中国期刊全文数据库(1979²013年)等数据库和相关会议论文集及查阅检索到的所有文献的参考文献,对纳入文献进行评价及资料提取。按照国际Cochrane协作网推荐的方法进行系统评价。结果共纳入22个试验包括1 649例患者。大多试验方法学质量较差且样本量小,Meta分析结果显示:(1)银杏叶提取物联合常规治疗与常规治疗的比较:能减少糖尿病肾病患者24 h尿微量白蛋白排泄率和24 h尿蛋白,能降低血清肌酐(P<0.000 01、P=0.002、P=0.001);(2)银杏叶提取物联合ACEI或ARB治疗与ACEI或ARB治疗的比较,能减少糖尿病肾病患者24 h尿微量白蛋白排泄率,能降低血清肌酐(P<0.000 1、P=0.04)。结论银杏叶提取物治疗糖尿病肾病有一定的疗效。但由于本系统评价纳入的试验样本量较小且方法学质量低下,现有的证据尚不足以推荐临床常规应用银杏叶提取物治疗糖尿病肾病,仍需大量循证医学证据的进一步积累,从而指导临床实践。     

2型糖尿病患者尿白蛋白排泄率与血脂的关系

目的探讨2型糖尿病患者尿白蛋白排泄率与血脂的关系。方法无尿路感染及原发性肾脏疾病病史的2型糖尿病患者68例,按尿白蛋白排泄率分为正常白蛋白尿组、微量白蛋白尿组和大量白蛋白尿组。检测所有患者的空腹血糖、糖化血红蛋白、血清甘油三酯、总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇。结果微量白蛋白尿组和大量白蛋白尿组空腹血糖、糖化血红蛋白、收缩压和舒张压均高于正常白蛋白尿组;大量白蛋白尿组的空腹血糖、糖化血红蛋白、收缩压和舒张压均较微量白蛋白尿组高。微量白蛋白尿组和大量白蛋白尿组血清甘油三酯、总胆固醇和低密度脂蛋白胆固醇水平均高于正常白蛋白尿组;大量白蛋白尿组血清甘油三酯、总胆固醇和低密度脂蛋白胆固醇较微量白蛋白尿组高。3组血清高密度脂蛋白胆固醇水平无统计学意义(P>0.05)。结论2型糖尿病患者尿白蛋白排泄率不仅与糖代谢指标和血压有关,与血脂也存在相关性,提示脂质代谢紊乱在糖尿病肾病的发生、发展中可能起一定的作用。     

缬沙坦联合氨氯地平治疗早期糖尿病肾病合并高血压疗效观察

目的研究血管紧张素Ⅱ受体阻滞剂(缬沙坦)单独和联合苯磺酸氨氯地平应用对Ⅱ型糖尿病肾病(DN)合并高血压患者降压疗效及其对尿蛋白排泄量的影响。方法 122例DN合并高血压患者随机分为2组,缬沙坦组(对照组)60例,给予缬沙坦80 mg,1次/d;观察组62例,给予左旋氨氯地平5mg及缬沙坦80 mg,1次/d。疗程均为12周。治疗后观察降压效果及尿蛋白排泄量的变化。结果 2组治疗后均能显著降低血压、空腹血糖、糖化血红蛋白,降低血尿素氮、肌酐及尿蛋白排泄量,但观察组降低血压及尿蛋白排泄量的幅度明显高于对照组(P<0.01)。结论缬沙坦单独和联合氨氯地平治疗DN合并高血压,均可明显降低血压,减少血尿素氮、肌酐及尿蛋白排泄量,保护肾功能,但与苯磺酸氨氯地平两药联用时降压作用及改善蛋白尿作用更好。     

Tranilast prevents the progression of experimental diabetic nephropathy through suppression of enhanced extracellular matrix gene expression

The present study was performed to investigate the effects of the antiallergic drug tranilast on the development of diabetic nephropathy in streptozotocin (50 mg/kg)-induced diabetic spontaneously hypertensive rats (SHR). Diabetic SHR were given standard chow or chow containing tranilast at a dose of 1400 mg/kg for 24 weeks. The effects of tranilast on urinary albumin excretion, mesangial expansion, expression of transforming growth factor-beta (TGF-beta) and type I collagen mRNAs, number of anionic sites on the glomerular basement membrane (GBM), and urinary TGF-beta and 8-hydroxy-2'-deoxyguanosine (8-OHdG) excretion were assessed. Tranilast did not affect the blood glucose concentration or blood pressure in diabetic SHR. Urinary albumin excretion rate and creatinine clearance were markedly increased in diabetic SHR. Tranilast treatment decreased albuminuria and hyperfiltration. Tranilast inhibited the diabetes-induced expansion of mesangial and tuft areas, as well as the increase in urinary TGF-beta and 8-OHdG excretion, loss of anionic sites of GBM, and overexpression of TGF-beta as determined immunohistochemically. The levels of TGF-beta and type I collagen mRNA expression were increased in the renal cortex in untreated diabetic SHR at 24 weeks, as determined by real-time quantitative polymerase chain reaction. Tranilast treatment inhibited the up-regulation of TGF-beta and type I collagen mRNA expression by 65 and 36%, respectively, in diabetic SHR. In conclusion, tranilast decreased albuminuria by suppressing glomerular hyperfiltration, mesangial expansion, and loss of the charge barrier via regulation of extracellular matrix gene expression and oxidative stress. Tranilast may be clinically useful in the treatment of diabetic nephropathy.     

Additive effects of Simvastatin beyond its effects on LDL cholesterol in hypertensive type 2 diabetic patients

BACKGROUND: Experimental evidence indicates that statins might have direct vascular effects independently from low-density lipoprotein (LDL) cholesterol reduction and we reported that the reduction in urinary albumin excretion rate during Simvastatin treatment in type 2 diabetic patients was not correlated with LDL-cholesterol decrease. However in humans there are no data regarding possible additional effects of Simvastatin on blood pressure and urinary albumin excretion beyond its capacity to lower serum cholesterol. PATIENTS AND METHODS: Twenty-six microalbuminuric hypertensive type 2 diabetic patients (diastolic blood pressure - after four months wash-out from the previous antihypertensive therapy - consistently > 90 and < 100 mmHg; plasma LDL-cholesterol > 3.9 and < 6.5 mmol L-1) were enrolled in the study. In random order, these patients received Simvastatin (20 mg day-1) or Cholestyramine (6 g three times a day) for a period of 10 months and after three months of wash-out (cross-over) the sequence was reversed for an additional 10 months. Blood pressure, lipid parameters, glycated haemoglobin and urinary albumin excretion were measured during the study. Additionally, in eight patients, urinary glycosaminoglycan excretion (GAG) was also measured during the study. RESULTS: Simvastatin and Cholestyramine were equally effective in reducing total and LDL cholesterol. Only during Simvastatin treatment a significant reduction in diastolic blood pressure and both 24 h urinary albumin and GAG excretion rates were observed, while no significant changes were seen with Cholestyramine treatment. CONCLUSIONS: Our results clearly show for the first time that the reduction of blood pressure, together with 24 h urinary albumin excretion rate - two established cardiovascular risk factors, obtained during Simvastatin therapy in hypertensive type 2 diabetic patients - is in large part independent from the reduction of LDL Cholesterol.     

Diabetic hypertensive patients. Is this a group in need of particular care and attention?

Morbidity and mortality in diabetes are caused mainly by its vascular complications, both in the microcirculation and in the large vessels. Diabetic nephropathy and retinopathy are the clinical hallmarks of microangiopathy, which may lead to end-stage renal failure and blindness. The cardiovascular complications in diabetes consist mainly of an accelerated form of atherosclerosis. Systemic hypertension is an early and frequent phenomenon. Nocturnal hypertension is also more frequent in people with diabetes compared with the nondiabetic population. Capillary hypertension has been demonstrated in type 1 diabetic patients. Poor metabolic control may induce elevation in blood pressure, but data are conflicting. The prevalence of white-coat hypertension in the diabetic population is comparable with that in the nondiabetic population. Prospective observational studies in type 1 and type 2 patients have revealed that abnormally increased urinary albumin excretion and other potentially modifiable risk factors--such as hypertension, smoking, poor metabolic control, and social class--predict increased all-cause mortality and cardiovascular mortality. Arterial hypertension is a risk factor in the initiation and progression of diabetic micro- and macroangiopathy. Diabetes, hypertension, and smoking are the three most important risk factors for fatal and nonfatal stroke. A randomized, double-blind, parallel study has revealed that the 5-year major cardiovascular disease rate was lowered by 34% for antihypertensive treatment compared with placebo. Furthermore, the study found a trend for lower all-cause mortality for low-dose antihypertensive-treated diabetic patients. Effective blood pressure reduction with ACE inhibitors and/or non-ACE inhibitors, frequently in combination with diuretics, reduces albuminuria, delays the progression of nephropathy, postpones end-stage renal failure, and improves survival in diabetic nephropathy.     

血D-二聚体、纤维蛋白原、同型半胱氨酸测定在糖尿病肾病中的意义

目的 探讨血D-二聚体（DD）、纤维蛋白原（FIB）、同型半胱氨酸（Hcy）测定在早期糖尿病肾病中的临床意义.方法 选择已确诊的2型糖尿病患者141例,健康对照组46例,测定清晨空腹血DD、FIB、Hcy水平.并同时收集糖尿病患者24h尿液进行尿微量白蛋白（mALB）测定,按照其24h尿白蛋白排泄率分为正常蛋白尿组（mALB≤30mg/24h）及微量蛋白尿组（mALB30-300mg/24h）.结果 2型糖尿病患者DD、FIB在正常蛋白尿组已升高;微量蛋白尿组三项指标均显著高于对照组,差异具有统计学意义（P〈0.01）,且三项联合检测阳性率明显高于单项检测.结论 联合检测DD、FIB、Hcy水平对观察糖尿病患者病情发展变化及提高糖尿病早期肾脏损伤的检出率具有重要的临床意义.     

血清总胆红素与2型糖尿病肾病的相关性研究

目的探寻血清总胆红素(TB)与2型糖尿病肾病的相关性。方法将126例住院2型糖尿病患者按尿白蛋白排泄率(UAER)将其分为正常蛋白尿组、早期糖尿病肾病组、临床糖尿病肾病组,比较三组血清TB水平及其他临床生化资料,探寻血清TB与UAER的相关性,并采用多因素Logistic回归分析探讨糖尿病肾病发病的影响因素。结果三组间年龄、体质量指数(BMI)、舒张压(DBP)、尿酸(UA)、总胆固醇(TCH)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、糖化血红蛋白(Hb A1c)比较差异均无统计学意义(P0.05),糖尿病病程、收缩压(SBP)、TB在不同组间差异有统计学意义(P0.05)。Spearman相关分析显示血清TB与UAER显著负相关(r=-0.32,P0.01)。Logistic多元回归分析显示BMI和TB是糖尿病肾病的独立影响因素(OR=1.189、0.850;P0.05、P0.01)。结论血清TB与2型糖尿病肾病呈负相关,其可能成为糖尿病肾病的一种新治疗靶点。     

灯盏细辛治疗糖尿病肾病的系统评价

目的系统评价灯盏细辛治疗糖尿病肾病（DN）的疗效及安全性。方法计算机检索Cochrane图书馆临床对照试验库、MEDLINE、EMbase、中同期刊全文数据库（CNKI）,中国生物医学文献数据库和中文科技期刊全文数据库,手工检索《中华内分泌代谢杂志》等14种相关中文期刊、相关会议记录及所获文献的参考文献。收集灯盏细辛治疗糖尿病肾病的随机或半随机对照试验。由两名研究者独立选择试验、提取资料,并按照Cochrane系统评价的方法评价纳入研究的质量和提取有效数据,而后应用RevMan5．0．18软件进行Meta分析。结果共纳入32个RCT和1个半随机试验,共计2322例DN患者。大部分试验方法质量学较低且样本含量小。“漏斗图”呈不对称分布,提示可能存在发表偏倚及试验方法质量低下,发表偏倚提示阴性结果的试验可能未发表。Meta-析结果显示：①灯盏细辛可减少糖尿病肾病的24小时尿白蛋白排泄率、24小时尿总蛋白、降低血清肌酐、血浆胆固醇、甘油三酯、血浆粘度及纤维蛋白原。②灯盏细辛在降低DN患者24小时尿白蛋白排泄率和血清肌酐方面与ACEI类药物的疗效相似,但窖低24小时尿蛋白总量效果不如ACEI。③灯盏细辛在减少DN患者24小时尿蛋白和血浆纤维蛋白原方面,疗效优于丹参。④灯盏细辛与凯时（前列腺素E1）相比,降低24小时尿白蛋白排泄率不如凯时。治疗期间尚未发现严重的不良反应。结论灯盏细辛可能是一种相对安全和有效治疗糖尿病肾病的药物。由于纳入试验方法质量低下和可能存在发表偏倚,使本系统评价的证据强度不足,有待进一步进行大样本、高质量的多中心随机双盲对照试验来证实。     

尿清蛋白与肌酐比值对2型糖尿病肾病的早期诊断价值

目的探讨测定尿清蛋白／肌酐比值对诊断早期糖尿病肾病的价值。方法选取105例2型糖尿病患者,其中包括45例早期糖尿病肾病患者,分别计算尿清蛋白／肌酐比值、24h尿蛋白定量及尿清蛋白排泄率,并比较它们之间的关系。结果早期糖尿病肾病组尿清蛋白／肌酐比值与24h尿蛋白定量及蛋白排泄率呈显著相关性（r=0．921,P〈0．01;r=0．857,P〈0．05）。结论尿清蛋白／肌酐比值是诊断早期糖尿病肾病的一项敏感且可靠的指标。     

Proteinuria in newly diagnosed type II diabetic patients

Urinary excretion of albumin, IgG, and beta 2-microglobulin was examined in 132 (69 men, 63 women) newly diagnosed, middle-aged type II diabetic patients and in 144 (62 men, 82 women) nondiabetic control subjects. Both male (N = 57) and female (N = 29) diabetic patients with normal urinary sediment showed an increased excretion of albumin compared with the respective nondiabetic subjects, and male diabetic patients also had an increased IgG excretion. No consistent difference was found in urinary beta 2-microglobulin concentration between the diabetic and nondiabetic subjects. In all, 19.5% of the diabetic subjects with normal urinary sediment (12 men, 5 women) showed urinary albumin concentration exceeding the highest value (35 mg/24 h) found in nondiabetic subjects without renal disease. The urinary excretion of albumin in the diabetic subjects was not associated with the presence of hypertension or coronary heart disease or with the fasting blood glucose or serum insulin levels measured at diagnosis of diabetes. In male diabetic subjects with urinary albumin excretion greater than 35 mg/24 h, a reduced creatinine clearance was found, suggesting the presence of structural damage associated with diabetic nephropathy. The early increase of urinary albumin excretion in type II diabetic patients may be mostly functional in nature. However, some patients may have structural renal damage associated with diabetic nephropathy present at diagnosis.