老年糖尿病肾病肾衰竭诊治进展

在世界大部分地区，DN是终末期肾病（ESRD）的首要病因。根据美国肾脏数据系统（USRDS）1996年资料，在ESRD病因中DN占36．39％，居首位；1997～2001年美国医保接受肾替代治疗的新增ESRD患者中，DN占第1位（45％），在日本（1998年）占35．7％。糖尿病（DM）患者发生ESRD在中老年（50～80岁）中概率最高。USRDS的数据显示，1型糖尿病（T1DM）和2型糖尿病（T2DM）2组发生率均很显著，     

重视糖尿病肾病的防治

社会经济的发展导致了某些不良生活方式的形成,与之相关的疾病谱中糖尿病发病率在全球范围内迅速增加。糖尿病肾病（DN）作为糖尿病最常见、最严重的慢性微血管并发症之一,其患病率随着糖尿病患病人数的增加也逐年增加。调查显示,我国1型糖尿病患者的DN累积患病率为30％～40％,2型糖尿病为15％～20％。由于2型糖尿病患病人数多,其所致DN人数明显多于1型糖尿病者。DN引发的终末期肾病（ESRD）已经成为威胁糖尿病患者生命的主要原因。在美国约40％的ESRD病人是由DN所致,每年新增ESRD患者中50％以上是由DN引发。在我国DN所致ESRD占总ESRD的8％左右,部分经济发达地区已增长至15％。DN导致的死亡在1型糖尿病患者中居首位,在2型糖尿病患者中也仅次于大血管并发症。     

糖尿病肾病治疗现状与展望

糖尿病肾病（DN）是糖尿病（DM）重要的微血管并发症，若不积极治疗，最终进展为终末期肾病（ESRD或ES-RF）。在西方国家，DN居ESRD原发疾病之首，约占25％～42％，我国DN约占ESRD的6％～10％。由于晚期DN的预防与治疗相当困难，所以从DM早期开始，有效防治DN的发生和发展已成为一项重要任务。     

糖尿病肾病患者肾功能的评估

糖尿病肾病（diabetic nephropathy，DN）是导致终末期肾脏疾病（ESRD）的常见原因。根据美国2007年度USRDS的报告，DN在ESRD中占43．8％，中国DN在ESRD中所占比例约为15％。更为严峻的是，DN患者发展进人终末期肾功能衰竭后，其’肾脏替代治疗的效果远较一般肾脏疾病差。     

丹参在防治老年糖尿病肾病中的价值

糖尿病肾病（diabetic nephropathy，DN）是糖尿病的最常见并发症，也是造成终末期肾病（endstage renal disease．ESRD）的主要原因。目前，在欧美发达国家透析患者巾．DN所致ESRD者占30％以上，国内这一比例也高达20％左右，且糖尿病发病率正以惊人的速度逐年递增，在美国，DN已超过高血压肾小动脉硬化成为ESRD的第一大主要原因。     

老年糖尿病肾病临床中药治疗最新进展

糖尿病肾病(DN)是糖尿病(DM)最常见并发症之一,发病率为20%～40%,DN已成为导致终末期肾病(ESRD)的首要致病因素〔1〕。一旦临床肾病发生,如不进行有效干预,几年之内肾小球滤过率逐渐下降,10年后50%,20年后75%以上的患者将发展为ESRD〔2〕。老年DN属中医消渴肾病范畴,是指     

糖尿病肾病的研究现状

糖尿病肾病(DN)是终末期肾病(ESRD)的主要病因，也是糖尿病的主要并发症和死亡原因。Skrivarhaug等研究显示，病程超过20年的1型糖尿病(T1DM)患者，临床肾病(ON)的患病率仅为7％(#942)，与日本Hugara等报道的平均病程为28年的T1DM患者DN的患病率为41％相差较大(#2678)。     

糖尿病肾病治疗进展

糖尿病肾病(DN)是糖尿病的慢性并发症,已逐渐成为终末期肾病(ESRD)的主要原因。临床上通过饮食治疗、强化血糖控制、加强血压控制、降低蛋白质、抗氧化应激等综合治疗,能够有效地延缓肾病的进展、减少ESRD的发生、改善DN患者的预后。     

盐酸吡格列酮对糖尿病肾脏的保护作用

随着全球代谢性疾病的流行，以胰岛素抵抗、肥胖和血糖代谢异常为特征的2型糖尿病的发生显著增加。目前，我国2型糖尿病患者约5000万～6000万人，仍有不断增加的趋势。长期慢性高血糖会引起大血管和微血管并发症，其中糖尿病肾病（diabetic nephropathy,DN）是常见的微血管病变，是当前导致终末期肾病（ESRD）的主要原因。     

糖尿病肾病进展为终末期肾病关键基因的筛选及与免疫细胞浸润关系

目的 利用生物信息学方法筛选糖尿病肾病（DN）进展为终末期肾病（ESRD）的关键基因，并探讨其与免疫细胞浸润的关系。方法 下载GSE142153数据集，包含23例DN患者（DN组）和7例由DN所致ESRD患者（ESRD组）的血液样本，共20 959个基因。筛选两组差异基因，分为上调和下调；通过加权基因共表达网络分析（WGCNA）鉴定DN进展为ESRD的关键模块。对差异基因及关键模块进行基因本体论（GO）和京都基因与基因组百科全书通路富集分析；将获得的差异基因及WGCNA关键模块基因分别输入STRING在线数据库，构建蛋白质—蛋白质相互作用（PPI）网络，采用MCC算法确定核心基因，并将两种方法获得的核心基因取交集，获得关键基因。采用受试者工作特征（ROC）曲线对获得的关键基因进行分析，计算曲线下面积（AUC），评价关键基因区分DN和ESRD的诊断效能。最后进行免疫细胞浸润分析，从Cibersort网站下载22个免疫细胞的基因表达矩阵，采用Cibersort反卷积算法计算出30个样本的22种免疫细胞的相对丰度，用来表示免疫细胞浸润情况，比较两组免疫细胞浸润情况；进一步采用Pearson法...     

糖尿病性心自主神经、末梢神经病变与糖尿病微血管并发症的关系

目的 观察糖尿病性心自主神经病变和末梢神经病变的患病率及其与其他糖尿病慢性并发症的关系。方法 利用心自主神经功能检测系统和神经电生理检测仪测定308例糖尿病患者（平均年龄49岁，平均HbA1c9.8%。平均病程14年）的心自主神经功能和肢体的末梢神经传导速度，皮肤痛温觉，振动觉，同时检测24h尿白蛋白排泄率和眼底视网膜照相。结果 糖尿病患者心自主神经病变患病率为47.1%。末梢神经病变患病率为54.2%,两者呈显著正相关。并与病程和糖尿病控制状况呈显著正相关。并发糖尿病性神经病变患者并发其他糖尿病慢性并发症的机率增高。结论 糖尿病性神经病变患病率较高，并与糖尿病其他慢性并发症密切相关。     

2型糖尿病肾病与血管紧张素转换酶基因多态性的研究

目的 探讨２型糖尿病肾病与ＡＣＥ基因Ｉ／Ｄ多态性。方法 应用ＰＣＲ方法检测了３６例健康对照者、５８例糖尿病肾病和５０例有糖尿病肾病、病程大于５年的２型糖尿病病人的ＡＣＥ基因Ｉ／Ｄ基因型。结果 三组间ＡＣＥ基因ＩＩ、ＩＤ、ＤＤ三种基因型和Ｉ、Ｄ两种等位基因的频率分布无显著性差异;在三种基因型之间,尿白蛋白排泄率和血肌酐水平也无显著性差异。结论 ＡＣＥ基因Ｉ／Ｄ多态生与中国汉族２型糖尿病肾病无关联,Ａ     

糖尿病患者530例足部状况的临床评估

目的对糖尿病患者足部状况及足溃疡发生相关因素进行临床评估.方法对530例糖尿病患者以自行设计的调查评价表对患者的一般临床资料、各项检查、化验指标、足部状况等与足溃疡相关内容进行评估.结果糖尿病患者的足部皮肤状况不良,糖尿病患者合并足溃疡发生率为14.34%,40%以上的糖尿病患者下肢大血管供血状况不良,有25%的糖尿病患者足部感觉异常,近50%的糖尿病患者处于足溃疡中度危险状态之中.结论糖尿病足发生的危险性与其神经病变、血管病变等并发症、足部不良状况、病程长、代谢紊乱等多种因素有密切的关系.     

Metabolomics window into diabetic complications

Diabetes has become a major global health problem. The elucidation of characteristic metabolic alterations during the diabetic progression is critical for better understanding its pathogenesis, and identifying potential biomarkers and drug targets. Metabolomics is a promising tool to reveal the metabolic changes and the underlying mechanism involved in the pathogenesis of diabetic complications. The present review provides an update on the application of metabolomics in diabetic complications, including diabetic coronary artery disease, diabetic nephropathy, diabetic retinopathy and diabetic neuropathy, and this review provides notes on the prevention and prediction of diabetic complications.     

Effect of probucol on triglyceride turnover in streptozotocin-diabetic rats

The long-term effect of probucol on triglyceride turnover was examined in streptozotocin (40 mg/kg) diabetic rats. Two diabetic groups were prepared: one group received a probucol-containing (1%) diet (probucol-treated diabetic) and the other standard diet (diabetic control). After 4 months of probucol diet, triglyceride turnover was estimated using Triton WR1339. In diabetic control rats, glucose, triglyceride and cholesterol concentrations in plasma and in the very low density lipoprotein (VLDL) fraction were markedly elevated and plasma insulin was suppressed compared to non-diabetic control rats. There was no significant difference in body weight, plasma glucose and insulin between the 2 diabetic groups. However, the probucol-treated diabetic group showed significantly suppressed levels of triglyceride and cholesterol in total plasma and in the VLDL fraction compared to each corresponding diabetic control value. On the other hand, there were no significant differences in triglyceride secretion rate between the 2 diabetic groups. Newly secreted VLDL particles after Triton injection from diabetic control rats were significantly cholesterol-enriched and triglyceride-depleted compared to those from non-diabetic control rats. However, the composition of those from probucol-treated diabetic rats was similar to that of non-diabetic control group. Prominent hypertriglyceridemia without increase in triglyceride secretion rate in diabetic control group indicates triglyceride removal defect in diabetic rats. Significant suppression of plasma triglyceride level without changes in the triglyceride secretion rate in the probucol-treated diabetic group suggests that probucol stimulated triglyceride removal in diabetic rats. Thus, probucol might normalize VLDL composition, thereby contributing to accelerated triglyceride removal from the circulation of streptozotocin diabetic rats without affecting glucose metabolism.     

Plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels in diabetic foot ulcers

Plasma TAFI may participate in arterial thrombosis in cardiovascular diseases (CVD) and may be involved in the mechanism of vascular endothelial damage in diabetic patients. The aim of this study was to investigate the association of plasma TAFI antigen level in the development of diabetic foot ulcer in Type 2 diabetes. The TAFI antigen levels were determined in 50 patients with diabetic foot ulcers and 34 patients without diabetic foot ulcers and 25 healthy individuals. We measured TAFIa/ai antigen in plasma samples with a commercially available ELISA Kit. Diabetic foot ulcer group and diabetic group were similar in terms of mean age and sex distribution. Diabetes duration, retinopathy, neuropathy, macrovascular disease and infection were related to diabetic foot ulcers. HbA1c, HDL-cholesterol and Folic Acid levels were decreased in the diabetic foot ulcer group. TAFI levels were 99.44?±?55.94% in control group, 135.21?±?61.05% in diabetic foot ulcer group, 136.75?±?59.38% in diabetic group and was statistically different (P??0.05). No significant difference in plasma TAFI levels were seen between diabetic foot ulcer stages. TAFI antigen levels are increased in Type 2 diabetic patients, but are not related to diabetic foot ulcer development.     

Heart triglyceride synthesis in diabetes: selective increase in activity of enzymes of phosphatidate synthesis

Heart triglyceride content increased in streptozotocin-induced ketotic diabetic rats. Insulin treatment of the diabetic rats reversed the heart triglyceride content to normal values. Triglyceride synthesis from radioactive glycerophosphate was studied in heart homogenates of control, ketotic diabetic and insulin-treated diabetic rats. There was an increased synthesis of triglyceride and its precursors in the ketotic diabetic state suggesting an increased substrate flow through the triglyceride synthetic pathway. Insulin treatment of the diabetic rats reverted the substrate flow to control values. These results showed a correlation between the in vivo heart triglyceride content and triglyceride synthesis in heart homogenates of control, ketotic diabetic and insulin-treated rats. Activity of the various enzymes catalyzing the synthesis of triglyceride from palmitate was assayed under optimal conditions. Activity of enzymes of phosphatidate synthesis was increased in the diabetic state and was reversible to control values following insulin treatment of the diabetic rats. There was no change in the activity of fatty acid thiokinase or phosphatidate phosphohydrolase or diglyceride acyltransferase either in the ketotic diabetic state or following insulin treatment. The results suggested that increased synthesis of triglycerides played a role in heart triglyceride accumulation in the diabetic state. Increase in the activity of the enzymes of phosphatidate synthesis contributed to the increased triglyceride synthesis in the heart homogenates of the diabetic rats.     

Effects of genetic hypertension on diabetic nephropathy in the rat--functional and structural characteristics

Streptozotocin (STZ) diabetes was induced in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. Body weight, blood pressure, renal function, glycaemic control and proteinuria were assessed monthly for 32 weeks. At 32 weeks, the animals were killed and glomerular basement membrane (GBM) thickness and fractional mesangial volume were measured. There was no significant difference in renal function between diabetic SHR and diabetic WKY. Diabetic SHR showed an earlier and larger rise in total proteinuria and urinary albumin excretion than diabetic WKY. Urinary albumin excretion was increased more than tenfold in diabetic SHR compared to diabetic WKY after 32 weeks of diabetes. GBM thickness was significantly increased in diabetic SHR compared with diabetic WKY. Both diabetic WKY and diabetic SHR showed mesangial expansion when compared to their nondiabetic counterparts. On the other hand, both hypertensive models showed increased glomerular volume, which was not influenced by the presence of diabetes. The diabetic SHR model has features of accelerated nephropathy, as evidenced by increased albuminuria and GBM thickness. This suggests that pre-existing hypertension may play an important role in the progression of diabetic renal disease.     

The number of glomeruli in Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic patients

Summary The number of glomeruli per kidney in Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic patients was estimated by an unbiased stereological method: the fractionator. No significant differences were observed between Type 1 and Type 2 diabetic patients without severe diabetic glomerulopathy and non-diabetic patients. Diabetic patients with proteinuria who were in the early stages of diabetic nephropathy also had a normal number of glomeruli. On the other hand, a subgroup classified as Type 1 diabetic patients with severe diabetic glomerulopathy had significantly less glomeruli compared with Type 1 diabetic patients with mild or no glomerulopathy. A probable explanation is that Type 1 diabetic patients lose glomeruli in relation to the progression of diabetic glomerulopathy. A more theoretical alternative is, however, that development of diabetic glomerulopathy is facilitated by a low number of glomeruli.Presented in part at the first meeting of the European Diabetic Nephropathy Study Group, Pisa, Italy, April 1988, and at the 23rd annual meeting of the Scandinavian Society for the Study of Diabetes, Bergen, Norway, May 1988     

结合珠蛋白基因多态性与糖尿病视网膜病变（一）

目的探讨结合珠蛋白（Hp）基因多态性与2型糖尿病（T2DM）患者糖尿病视网膜病变（DR）发病的关系。方法将317例T2DM患者分为糖尿病无视网膜病变（NDR）组和DR组,并选取100名正常人作为对照（NC）组。采用PCR技术扩增Hp1和Hp2特异的目的片段,分析Hp基因型及糖尿病（DM）病程、尿白蛋白（UAlb）等生化指标与DR的关系。结果NDR组、DR组和NC组间Hp等位基因和基因型频率比较,均无统计学差异（P〉0．05）。经Logistic回归分析显示,DM病程和24hUAlb是DR的独立危险因素,Hp可能与DR无相关性。结论Hp基因多态性可能与DR无相关性,而DM病程和24hUAlb是DR的独立危险因素。