糖尿病肾病与糖尿病视网膜病变的相关性研究进展

糖尿病肾病(DN)和糖尿病视网膜病变(DR)均是糖尿病的微血管病变，是目前成人终末期肾病(ESRD)和致盲的重要原因，两者在发生、发展过程中具有一定平行性，又存在不平行性。DN和DR可预测彼此的发生、发展，但目前对于两者之间的关系尚未明确。因此，本文就DN与DR之间的相关性的研究进展作一综述，为临床诊断治疗提供帮助。     

糖尿病肾病肾小管间质病变研究进展

糖尿病肾病(DN)是糖尿病重要的慢性并发症，是终末期肾衰竭的主要原因之一。以往对DN的研究大多集中在肾小球病变，而对糖尿病状态下占据整个肾脏体积几乎达90%的肾脏小管间质病变的发生发展及其机制的研究却极为有限。     

糖尿病肾病早期诊断指标研究进展

糖尿病肾病(DN)是糖尿病的远期并发症之一。由于DN早期的临床症状常不明显,当出现临床症状时病变已不可逆转,故DN的早期诊断对DN的预后非常重要。本文结合国外近三年有关DN的最新研究进展,简要介绍了尿微量白蛋白、nephrin、血管内皮生长因子等在DN早期诊断中的作用及意义。     

降钙素基因相关肽与糖尿病肾病

降钙素基因相关肽(CGRP)是目前已知体内最强的舒血管多肽，属于降钙素基因肽超家族，参与许多重要功能的调节，糖尿病肾病(DN)是胰岛素依赖型和非胰岛素依赖型糖尿病的一种常见的微血管并发症，通过对CGRP与DN微血管病变的发病机制之间的研究，可能为DN的诊断和治疗带来新的手段。     

2型糖尿病肾病和糖尿病性视网膜病变的相关性研究

目的探讨2型糖尿病肾病和糖尿病性视网膜病变的发病机制及其两者之间的相关性。方法选择2004年1月至2014年12月北京中日友好医院肾内科经肾穿刺活检确诊的2型糖尿病肾病(diabetic nephropathy,DN)患者95例,按照肾脏病理改变程度分为5组,即DNⅠ组10例,DNⅡa组12例,DNⅡb组16例,DNⅢ组54例,DNⅣ组3例;将不同组间视网膜病变进行比较,分析视网膜病变与肾脏损伤之间的关系,以及视网膜病变与常用临床指标[24 h尿蛋白定量、空腹血糖(fasting blood glucose,FBG)、糖化血红蛋白(glycosylated hemoglobin,HbA1c)、血肌酐(SCr)及肌酐清除率(creatinine clearance rate,Ccr)]之间的关系。结果 DN患者肾脏损伤病理分型与视网膜病变呈正相关(r=0.458,P=0.016),但仍有23.2%患者无视网膜病变,分别发生在80.00%的DNⅠ组、33.33%的DNⅡa组、12.50%的DNⅡb组、14.81%的DNⅢ组患者中。临床指标中仅24 h尿蛋白定量与糖尿病视网膜病变的发生和发展相关。结论尽管糖尿病性视网膜病变常被提示DN,但少部分DN不存在视网膜病变的情况也应被重视。     

糖尿病肾病的蛋白质组学研究进展

糖尿病肾病(DN)是糖尿病最常见的微血管并发症,也是导致终末期肾病(ESRD)的重要原因。微量白蛋白尿作为预测DN进展的指标并不可靠,寻找DN早期生物学标志物以及对DN早期肾脏病变的机制研究为目前研究的重点。蛋白质组学技术近年来飞速发展,对DN患者的尿液、血液以及肾组织的蛋白质组学研究可能会为我们早期诊治DN提供新的希望。本文对蛋白质组学主要技术及DN蛋白质组学研究的近期研究进展进行综述。     

糖尿病肾病早期诊断指标研究进展

糖尿病肾病（DN）是糖尿病的远期并发症之一。由于DN早期的临床症状常不明显，当出现临床症状时病变已不可逆转，故DN的早期诊断对DN的预后非常重要。本文结合国外近三年有关DN的最新研究进展，简要介绍了尿微量白蛋白、nephrin、血管内皮生长因子等在DN早期诊断中的作用及意义。     

降钙素基因相关肽与糖尿病肾病

降钙素基因相关肽(CGRP)是目前已知体内最强的舒血管多肽,属于降钙素基因肽超家族,参与许多重要功能的调节,糖尿病肾病(DN)是胰岛素依赖型和非胰岛素依赖型糖尿病的一种常见的微血管并发症,通过对CGRP与DN微血管病变的发病机制之间的研究,可能为DN的诊断和治疗带来新的手段。     

2型糖尿病伴发非糖尿病性肾小球病变20例分析

糖尿病肾病是糖尿病的远期并发症之一,是糖代谢紊乱所致肾脏微血管病变的结果,具有独特的病理和临床特点.蛋白尿是糖尿病肾病(DN)最常见的临床表现之一 ,但是并非所有出现蛋白尿或者肾脏损害的糖尿病患者均属于DN.随着肾活检的开展,人们逐渐发现部分糖尿病患者的肾脏病变与糖尿病无关,而部分患者可以在糖尿病肾病的基础上同时合并其他的肾脏疾病,这就是所谓的糖尿病合并非糖尿病性肾脏疾病(NDRD).NDRD与DN 在病变性质,临床表现、治疗方法及预后均存在差异,本文通过对本院肾脏科近5年收治的2 0例NDRD患者的临床特点分析,以求提高对DM患者出现肾脏损害时的诊断与鉴别诊断水平, 为这类患者提供有效的诊治方案.     

终末期糖尿病肾病患者CRRT治疗过程中应注意的问题

近十年来糖尿病肾病(DN)所导致终末期肾病(ESRD)在我国呈明显增长趋势，其中绝大部分需要接受肾脏替代治疗(CRRT)。这类病人无论从疾病所涉及的范围和程度，还是原发病进展的速度均与非糖尿病性肾病明显不同。突出表现在DN所合并的夹杂症较多，随时能危及生命，如心肌梗死(心梗)、充血性心衰、猝死、脑卒中等。其次，有些合并症(如末梢血管阻塞、视网膜病变、糖尿病足、神经系统病变、频发感染及脂质代谢紊乱等)能明显加速病情的进展。除此之外，DN患者在透析过程中，不仅高血压顽固，难以控制，残余肾功能也较非DN病人丧失的更快；血糖调整也较为困难，极易发生低血糖反应；还由于高糖透析液的缘故.     

Classification of diabetic retinopathy and diabetic macular edema

The global incidence and prevalence of diabetes mellitus (DM) have reached epidemic proportions. Estimates indicate that more than 360 million people will be affected by DM by 2030. All of these individuals will be at risk of developing diabetic retinopathy (DR). It is extremely important to categorize, classify and stage the severity of DR in order to establish adequate therapy. With proper management more than 90% of cases of visual loss can be prevented. The purpose of the current paper is to review the classification of DR with a special emphasis on the International Clinical Disease Severity Scale for DR. This new classification is simple to use, easy to remember and based on scientific evidence. It does not require specialized examinations such as optical coherence tomography or fluorescein angiography. It is based on clinical examination and applying the Early Treatment of Diabetic Retinopathy Study 4:2:1 rule.     

Enzymatic vitrectomy for diabetic retinopathy and diabetic macular edema

The aim of this paper is to determine the role of enzymatic vitrectomy performed by intravitreal injection of autologous plasmin enzyme (APE) in the management of diabetic retinopathy and diabetic macular edema (DME). Diabetic patients with proliferative diabetic retinopathy or DME and evident posterior hyaloid adherence to the retinal surface were included. All cases were treated with an initial intravitreal injection of APE and reevaluated one month later, measuring changes in best-corrected visual acuity (BCVA), macular thickness and the status of the posterior hyaloid. A second APE injection was performed in cases with no evident posterior vitreous detachment (PVD) after the initial treatment. Sixty-three eyes were included in the present review. A complete PVD appeared in 38% of cases (24 eyes) after one injection of plasmin and the total increased to 51% (32 eyes) after the second injection, separated at least by one month. The central macular thickness improved in all cases (100%) and BCVA in 89%. Finally, in 50% of eyes with proliferative diabetic retinopathy, a high reduction of new vessels regression was observed. Enzymatic vitrectomy could be considered a good therapeutic alternative in diabetic retinopathy and macular edema.     

糖尿病周围神经病变在糖尿病骨病中的发病机制研究进展

糖尿病骨病是指糖尿病患者出现骨质减少、关节病变、骨皮质变薄、骨骼脆性增加甚至骨折的一种全身性、代谢性骨病,是糖尿病的重要并发症之一。随着糖尿病患者生活质量的提高以及病程的延长,患者的肌肉骨骼病变发生率在逐年提高,严重者可导致残疾或死亡。其发病机制目前尚未完全阐明,近年来,随着对糖尿病骨病的深入研究,发现糖尿病周围神经病变在骨骼疾病的发病和进展中起着重要作用。本文就糖尿病骨病、神经病变之间的关系加以综述,旨在探索神经病变导致骨代谢失调、骨密度下降、骨折风险的可能机制,为糖尿病骨病的诊断、预防、治疗提供新思路。     

Development of late-stage diabetic nephropathy in OVE26 diabetic mice

OVE26 mice are a transgenic model of severe early-onset type 1 diabetes. These mice develop diabetes within the first weeks of life and can survive well over a year with no insulin treatment, and they maintain near normal body weight. To determine whether OVE26 mice provide a valuable model of chronic diabetic nephropathy (DN), OVE26 diabetic mice were compared with their nondiabetic littermates for functional and structural characteristics of DN. OVE26 mice exhibited pronounced polyuria and significant albuminuria by 2 months of age (305 microg/24 h in OVE26 vs. 20 microg/24 h in controls). Albumin excretion rate increased progressively with age and exceeded 15,000 microg/24 h at 9 months of age. The profound loss of albumin led to hypoalbuminemia in some diabetic animals. Albuminuria coincided with an elevation in blood pressure as measured by tail cuff. The glomerular filtration rate (GFR) in OVE26 mice measured using fluorescein isothiocynate inulin clearance demonstrated that GFR increased significantly from 2 to 3 months of age and then decreased significantly from 5 to 9 months. GFR in 9-month-old diabetic mice was significantly lower than that of 9-month-old control mice. The decline in GFR coincided with a significant increase in renal vascular resistance. Structural studies showed an almost twofold increase in kidney weight between 2 and 5 months. Diabetic mice also showed progressively enlarged glomeruli and expanded mesangium with diffuse and nodular expansion of mesangial matrix. Tubulointerstitial fibrosis was also observed in these mice. Glomerular basement membrane was thickened in OVE26 mice. In summary, OVE26 mice demonstrate that most of the characteristics of human DN can be produced by chronic hyperglycemia in a murine model. This model will be useful for improved understanding and treatment of DN.     

Painful diabetic neuropathy

The podiatric physician often encounters complex painful neuropathies in daily practice. Diabetic neuropathy is one form of chronic neuropathic pain dealt with on a regular basis. The goal of this article is to review the pathophysiology, diagnosis, and treatment options of this complaint. Medical and surgical interventions are discussed, with a clinical emphasis on patient selection and prevention.