替米沙坦对大鼠糖尿病肾病中PPARγ途径的作用

目的 观察替米沙坦对大鼠糖尿病肾病中PPARγ途径的作用.方法 予替米沙坦治疗大鼠糖尿病肾病.结论 替米沙坦可能通过PPARγ途径对糖尿病肾病中肾脏损伤起保护作用.     

天然黄酮类化合物防治糖尿病肾病的研究进展

糖尿病肾病（DN）是一种严重的糖尿病并发症,其发病机制复杂而多样。现代药理研究表明,天然黄酮类化合物具有多种潜在药用价值,对糖尿病肾病的防治作用就是其中之一。黄酮类化合物抗糖尿病肾病的作用机制是多方面药理活性的综合结果,包括通过抗氧化应激与清除自由基、抗炎、改善血糖血脂紊乱、抗凋亡、调节血管舒张及改善血流动力学异常等途径来实现。在查阅近年来国内外发表的相关文献后,对黄酮类化合物在糖尿病肾病防治中的多种作用及相关机制进行综述,以期为糖尿病肾病防治药物的研发提供参考。     

辛伐他汀对糖尿病肾病患者IL-18及尿白蛋白排泄率的影响

通过检测糖尿病肾病患者辛伐他汀治疗前后血清IL-18水平的变化,以及与正常对照组的比较,表明IL-18在糖尿病肾病的发病过程中起着重要作用,辛伐他汀治疗糖尿病肾病的机制可能是通过抑制IL-18的表达实现的。     

氧化应激与糖尿病肾病

糖尿病肾病是糖尿病严重的并发症，至今其发病机制尚未完全阐明，目前认为氧化应激可能起重要作用。本文就氧化应激与糖尿病肾病的关系做一综述。     

中药有效成分防治糖尿病肾病的实验研究进展

从中药中寻找有效成分是研制治疗糖尿病肾病的新药的一条重要的途径,近年来不论是中医药治疗糖尿病及其肾病并发症的临床运用,还是有关中药有效成分在防治糖尿病肾病方面的实验研究均取得了较大进展,特别是中药有效成分防治糖尿病的作用机制研究.该文就中药有效成分防治糖尿病肾病的实验研究近况作一综述,旨在为开展单一成分的临床研究和新的中药制剂开发应用提供参考.     

利格列汀结合舒洛地特治疗对糖尿病肾病患者血管内皮细胞生长因子影响的研究

<正>糖尿病肾病是糖尿病血管并发症中较为常见的慢性并发症之一,同时也是糖尿病患者致残、致死的关键原因~([1,2])。据相关统计资料显示,我国每年由1型、2型糖尿病进展转化为糖尿病肾病的患者占据20%~40%左右,且大部分糖尿病肾病患者后期可能进展为肾脏疾病,需长期坚持透析治疗或接受肾脏移植手术来维持生命~([3,4])。目前临床上尚未明确其发病机制,有大量文献提示糖尿病肾病患者早期可能出现肾脏微     

30例糖尿病肾病患者血同型半胱氨酸水平的升高及其意义

目的：阐明糖尿病肾病发病机制。方法：用高压液相萤光检测法测定。结果：糖尿病肾病组血同型半胱氨酸的水平显著高于正常对照组。结论：高同型半胱氨酸可能通过损害血管内皮，刺血管平滑肌增殖，从而在糖尿病肾病发病机制中起重要作用。     

活性维生素D3与糖尿病肾病的关系研究进展

糖尿病肾病是糖尿病的主要并发症和终末期肾脏疾病的主要死亡原因之一,目前尚无有效地预防及治疗手段.研究显示活性维生素D3对肾脏具有保护作用,其作用机制可能是通过抗炎及抗纤维化实现的.该文对近年来国内外关于活性维生素D3对糖尿病肾病的保护机制及临床治疗进行了综合分析,这对于预防和寻找新的治疗糖尿病肾病方法具有重要意义.     

小檗碱预防性治疗糖尿病肾病的研究进展

糖尿病肾病是糖尿病微血管并发症之一,其发病机制复杂,与糖脂代谢紊乱、炎症、氧化应激、自噬受损、肠道菌群失调等因素交叉关联,也是导致终末期肾病的主要原因。综述了糖尿病肾病的主要发病机制以及小檗碱预防性治疗糖尿病肾病的研究进展,旨在为糖尿病肾病治疗药物的研发提供参考。     

中药延缓糖尿病肾病肾小球硬化的作用机制

糖尿病是中老年的常见病,在我国,每年的患病人数成增长的趋势。如果糖尿病未能及时控制,就可能会逐渐损害肾脏,引起糖尿病肾病。中西药联合治疗糖尿病已经有了很大的成果,特别是中医,能够弥补西医的很多不足,更好地改善患者的体质和生存质量。本文主要对中药延缓糖尿病肾病肾小球硬化的可能作用机制进行报道如下。     

Treatment of type 2 diabetic nephropathy by blockade of the renin-angiotensin system: a comparison of angiotensin-converting-enzyme inhibitors and angiotensin receptor antagonists

Type 2 diabetes is the most prevalent form of diabetes mellitus worldwide and associated diabetic nephropathy is the most common cause of end-stage renal disease in the USA. Lowering blood pressure and controlling glucose slows the progression to end-stage renal disease or death. Although angiotensin-converting-enzyme inhibitors reduce proteinuria, their effects to slow progression to end-stage renal disease have not been clearly demonstrated in type 2 diabetic nephropathy. Recent clinical trials with angiotensin AT(1) receptor antagonists demonstrate that they reduce proteinuria, stabilize renal function and slow the progression of nephropathy to end-stage renal disease in patients with type 2 diabetes. These are significant benefits beyond those associated with conventional therapy and blood pressure control.     

microRNAs 在糖尿病肾病发病机制中的作用

近年研究发现微小 RNA （miRNAs） 是转录后基因调控的关键因素, 参与诸多疾病的发生、 发展。在肾脏病研究中, miRNAs 的作用也日益受到重视。糖尿病肾病 （DN） 是终末期肾脏病的主要原因之一, 发病机制尚未完全阐明。本文就 miRNAs 在 DN 发病机制中的作用进行综述。     

Molecular mechanisms of diabetic nephropathy and its therapeutic intervention

Diabetic nephropathy is a leading cause of end-stage renal failure, which could account for disabilities and high mortality rates in patients with diabetes. Diabetic nephropathy seems to occur as a result of an interaction between metabolic and hemodynamic factors, which activate common pathways that lead to renal damage. Recent large landmark clinical studies have shown that intensive glucose control reduces the risk of the development and progression of diabetic nephropathy, and the blockade renin-angiotensin system (RAS) is also an important target for both metabolic and hemodynamic derangements in diabetic nephropathy. However, diabetic nephropathy remains the leading cause of end-stage renal failure in developed countries. Therefore, to develop novel therapeutic strategies that specifically target diabetic nephropathy may be helpful for most patients with diabetes. High glucose, via various mechanisms such as increased production of oxidative stress and advanced glycation end products (AGEs), and activation of the RAS and protein kinase C (PKC), elicits vascular inflammation and alters gene expression of growth factors and cytokines, thereby it might be involved in the development and progression of diabetic nephropathy. This article summarizes the molecular mechanisms of diabetic nephropathy and the potential therapeutic interventions that may prevent this devastating disorder even in the presence of hyperglycemia, control of which is often difficult with current therapeutic options.     

糖尿病肾病相关药物研究进展

糖尿病肾病(DN)是糖尿病重要微血管并发症,其病理特征性表现为肾小球周边部位出现嗜酸性K-W结节,是糖尿病性肾病具有诊断意义的改变。但仅出现于约10%～20%的糖尿病性肾病患者。糖尿病性肾病其他病理改变特点包括肾小球基膜增厚,肾小球上皮细胞足突融合以及由于细胞外系膜基质增多所致肾小球增大。疾病晚期可出现肾小管萎缩肾内纤维化。糖尿病病程10年以上者约50%并发糖尿病肾病,每年新增终末期肾病中,糖尿病导致者所占比例逐年增高。近年关于血管紧张素转换酶抑制剂(ACEI)治疗糖尿病肾病的研究较多。其外内皮素拮抗剂等,被认为有一定的肾脏保护作用,基因治疗亦给糖尿病肾病带来新希望。现就有关内容综述如下。     

临床研究中的新型糖尿病肾病药物

糖尿病肾病（diabetic nephropathy,DN）是糖尿病最常见、最严重的并发症之一,也是导致终末期肾功能衰竭的重要原因之一。糖尿病肾病发病机制非常复杂,是在遗传背景的基础上多因素综合作用的结果。近年来研究表明,氧化应激、炎症反应以及多种致纤维化细胞因子的联合作用在DN的发生发展中具有极为重要的意义,并进一步导致肾脏纤维化,最终发展为DN。DN具有发病率高、治疗困难、预后差等特点,目前尚无特别有效的针对性疗法,因此,各大药物公司都在糖尿病肾病方面投入大量研究,并且取得了一定成果,发现了一些治疗DN的新型药物。本文将介绍一些处于临床研究中的新型DN药物。     

Quercetin, an anti-oxidant bioflavonoid, attenuates diabetic nephropathy in rats

1. Diabetic nephropathy is an important microvascular complication and one of the main causes of end-stage renal disease. Many in vivo and in vitro studies have indicated that oxidative stress is one of the major pathophysiological mechanisms involved in the development of diabetic nephropathy. In the present study, we examined the effect of an anti-oxidant bioflavonoid quercetin on renal function and oxidative stress in streptozotocin (STZ)-induced diabetic rats. 2. Diabetes was induced in Sprague-Dawley rats with a single intravenous injection of STZ (45 mg/kg). Four weeks after STZ injection, quercetin (10 mg/kg per day) was given orally for 4 weeks in both control and diabetic rats. Plasma glucose levels and bodyweights were measured at 4 and 8 weeks after the STZ injection. At the termination of the experiments, urine albumin excretion, urine output, serum creatinine, blood urea nitrogen, creatinine and urea clearance were measured. The renal oxidative stress marker malonaldehyde, glutathione levels and the anti-oxidant enzymes superoxide dismutase and catalase were measured in kidney homogenate. 3. Streptozotocin-injected rats showed significant increases in blood glucose, polyuria, proteinuria and a decrease in bodyweight compared with age-matched control rats. After 8 weeks, diabetic rats exhibited renal dysfunction, as evidenced by reduced creatinine and urea clearance, and proteinuria along with a marked increase in oxidative stress, as determined by lipid peroxidation and activities of key anti-oxidant enzymes. Treatment with quercetin significantly attenuated renal dysfunction and oxidative stress in diabetic rats. 4. These results confirm the role of oxidative stress in the development of diabetic nephropathy and point to the possible anti-oxidative mechanism being responsible for the nephroprotective action of quercetin.     

New approaches for treatment of diabetic nephropathy: the endothelium as a target for drug discovery

Diabetic nephropathy is the leading cause of end-stage renal disease (ESRD). There are currently no therapeutic Hyperlipidaemiants which directly intervene in the pathogenesis of diabetic nephropathy. The mechanisms behind development of diabetic nephropathy are complex and not completely understood. The hyperglycaemia, hyperlipidaemia and hyperinsulinaemia found in diabetics might all act on the kidney endothelium to induce expression of genes important in kidney dysfunction. We propose that targeting kidney endothelial gene expression may provide a new approach for control of kidney dysfunction.     

New approaches for treatment of diabetic nephropathy: the endothelium as a target for drug discovery

Diabetic nephropathy is the leading cause of end-stage renal disease (ESRD). There are currently no therapeutic Hyperlipidaemiants which directly intervene in the pathogenesis of diabetic nephropathy. The mechanisms behind development of diabetic nephropathy are complex and not completely understood. The hyperglycaemia, hyperlipidaemia and hyperinsulinaemia found in diabetics might all act on the kidney endothelium to induce expression of genes important in kidney dysfunction. We propose that targeting kidney endothelial gene expression may provide a new approach for control of kidney dysfunction.     

Treatment for diabetic nephropathy - a review of the recent patent literature

Diabetic nephropathy is now the leading cause of end-stage renal disease in the Western world. Renal disease develops secondary to long-standing hyperglycemia and hemodynamic alterations, which activate a common pathway that ultimately leads to the renal damage. Current strategies to treat diabetic nephropathy include optimization of glycemic control and treatment of glomerular and systemic hypertension. Although these strategies can slow the progression of proteinuria and decline in renal function, diabetic nephropathy remains a huge clinical problem. It is anticipated that future treatment modalities for preventing and treating diabetic nephropathy will involve drugs that modulate common pathogenetic pathways, possibly acting to inhibit both metabolic and hemodynamically induced forms of renal injury. These include inhibitors of growth factor and cytokine release or action, and inhibitors of intracellular second messengers. Although most of these agents have only been investigated in vitro, in animal experiments, or in relatively short-term human studies, these studies suggest that therapeutic strategies which involve a multifactorial approach may be more successful in the treatment of diabetic kidney disease than drugs which influence only one pathway.     

血液透析治疗糖尿病终末期肾病临床体会

目的探讨糖尿病肾病终末期患者的血液透析时机及并发症的防治。方法观察糖尿病终末期肾病（ESDN）及非糖尿病终末期肾病（NOR-ESDN）血液透析患者首次透析前血尿素氮、肌酐以及透析期间并发症、存活率。结果糖尿病终末期肾病血透患者的存活率较非糖尿病终末期肾病血透患者短,心血管并发症及感染并发症较NOR-ESDN血透患者发生多。结论 ESDN患者透析时机的选择应早于NOR-ESDN患者,应积极预防和控制并发症。