肝细胞生长因子与肾脏疾病

肝细胞生长因子（HGF）是一种多效应因子，具有诱导有丝分裂，促进运动和形态形成，并且有抗凋亡的作用。已经证实HGF是一强的肾营养因子，可以促进受损肾脏的再生和肾功能的恢复，具有广阔的治疗前景。     

糖尿病肾脏疾病生物标记物的研究进展

糖尿病肾脏疾病(DKD)是糖尿病常见的并发症之一,也是终末期肾病的主要原因。由于治疗手段有限,DKD的早期诊断和病程预测对于改善临床管理尤为重要。尽管蛋白尿、血肌酐等被认为是DKD早期诊断、病程评估的重要指标,但实际上它们的诊断效能非常有限。因此,亟需寻找更具诊断或预测价值的DKD生物标记物。本文就近年来DKD生物标记物的研究新进展作一综述,为诊断策略的开发提供思路。     

215例性发育异常疾病的分类比较研究

目的了解性发育异常疾病谱的变化,检验葛氏性发育异常疾病分类法的实用性和有效性。方法统计北京协和医院1996至2006年间性发育异常215例,根据葛氏性发育异常疾病分类法进行分类,并与1994年性发育异常疾病谱和性腺肿瘤发生率进行比较分析。结果215例性发育异常均能按葛氏性发育异常疾病分类法归人性染色体、性腺与性激素异常三大类;11年期间发生率较高的是性激素异常类性发育异常疾病。结论葛氏性发育异常疾病分类法是一种实用、简单、开放的分类法,并将随着对性发育异常疾病的认识而不断充实、发展。近年来性发育异常疾病的疾病谱和性腺肿瘤发生率也发生了一定的改变。     

TGF-β/Smad信号通路与肾脏疾病的研究进展

TGF-β(transforming growth factor-β)超家族成员主要有TGF-βs、活化素(activin)／抑制素(inhibins)、果蝇(Drosophila)的Dpp(Dccapentaplegic complex)、骨形态发生蛋白(BMP)等，它们对胚胎发育、器官形成、细胞的增殖、分化、凋亡起着重要的调节作用。TGF-β信号从细胞膜传人细胞核，与基因表达偶联，依赖Smads家族蛋白调节．     

肾脏的发育及疾病的功能基因组学研究

近五十年来,发育生物学家已经研究了肾脏发育的有关形态发生的过程.然而,随着转基因小鼠的出现,基因组测序和功能基因组的出现,关于肾脏发育的基因组学方面的理解也越来越值得关注.而且许多疾病都是由肾脏发育缺陷造成的,比如肾炎综合症、肾脏发育异常、新生儿肾脏肿瘤.本文将讨论新的基因组方法 的出现是怎样促进对肾脏发育和肾脏疾病的...     

雌激素与肾脏疾病的研究进展

雌激素(Estrogen)除调节人体生长发育和生殖外,在心血管、肿瘤、骨代谢等方面还具有广泛的生物学效应.本文就近年来雌激素在肾脏疾病领域中的研究进展作一简单概述.     

新生儿先天性肾脏和尿路发育异常的超声筛查及随访管理

目的 先天性肾脏和尿路发育异常是导致儿童慢性肾衰竭的首要原因,及早发现和诊断严重先天性泌尿系统畸形有助于防治并减少慢性肾衰的发生.本文通过在新生儿期对高危儿进行超声筛查,了解肾脏和尿路发育异常的发生情况,达到早期诊断的目的.方法 以随州市妇幼保健院为筛查中心,对高危儿行泌尿系统超声检查,对超声筛查异常者进一步检查,对符合转诊标准者转三级医院就诊,对不符合转诊者建立档案,定期随访.结果 高危儿超声筛查共479例,其中男289例（占60.33%）,女190例（占39.61%）,超声检查异常者69例（占14.4%）.超声检查异常患儿69例中男51例（占73.9%）,女18例（占26.1%）;其中肾盂积水68例,肾脏包块1例;左侧肾积水45例,右侧5例;双侧18例,4例伴左侧输尿管扩张;另有6例转诊至三级医院进行检查治疗.结论 高危新生儿期进行超声筛查可以早期发现先天性肾脏和尿路发育异常,对其进行及时干预和随访管理对防治先天性肾脏和尿路发育异常导致的儿童慢性肾衰竭有重要意义.     

肝细胞生长因子及其与肾脏疾病的关系

近年来,肝细胞生长因子在肾脏疾病中的作用正日益受到关注。本文对肝细胞生长因子合成的调控及其受体c-met信号转导等方面的进展作一介绍,并综述了近年国外关于肝细胞生长因子在急/慢性肾功衰,糖尿病肾病,肾小球肾炎等肾脏疾病或动物模型中的表达及作用方面的研究进展,提示肝细胞生长因子可能是一种有效的治疗某些肾脏病及估计预后的方法。     

TGF—β与肾脏疾病的研究新进展

转化生长因子（ＴＧＦ－β）与发育形成和组织的创伤修复有关,并参与机体免疫功能的调节和肿瘤发生,其过度生成可导致多种器官的纤维化。本文综述了ＴＧＦ－β的结构,功能及其与肾脏疾病关系方面的研究进展,并探讨了抗ＴＧＦ－β的临床治疗前景。     

单核细胞与高密度脂蛋白比值与糖尿病肾脏疾病的相关性研究

目的探讨单核细胞与高密度脂蛋白比值(monocyte to high-density lipoprotein cholesterol ratio,MHR)与糖尿病肾脏疾病(diabetic kidney disease,DKD)的关系。方法选取2018年6月至2019年6月于南京医科大学附属南京医院肾脏科住院的DKD患者140例,根据尿白蛋白肌酐比值分为A1组(30 mg/g)48例、A2组(30～300 mg/g)56例和A3组(30 mg/g)36例,比较各组临床资料,包括性别、年龄、肌酐、尿素、尿酸、三酰甘油、总胆固醇、胱抑素C、高密度脂蛋白、低密度脂蛋白、糖化血红蛋白、MHR等指标以及是否合并冠心病、高血压病等疾病。结果与A1组相比,A2组及A3组患者的TG、Scr、BUN、LDL、MHR升高,合并高血压病、冠心病比例增加,HDL水平较低(P0.05)。与A1组相比,A3组Scr、BUN、LDL、MHR升高,合并高血压病比例增加,而HDL降低(P0.05)。Logistic回归分析提示,矫正年龄、性别、病程、血白蛋白后,结果显示LDL、MHR、Scr、合并高血压病是DKD进展的独立危险因素(P0.05)。采用ROC曲线分析发现,MHR的曲线下面积最大,其截断值取0.396时,灵敏度为85.1%,特异度为68.8%。结论 MHR可以作为DKD进展的危险因素,在临床上对于MHR0.396的DKD患者,需进一步行相关检查,有助于监测及治疗DKD。     

HDAC inhibitors in kidney development and disease

The discovery that histone deacetylase inhibitors (HDACis) can attenuate acute kidney injury (AKI)-mediated damage and reduce fibrosis in kidney disease models has opened the possibility of utilizing HDACis as therapeutics for renal injury. Studies to date have made it abundantly clear that HDACi treatment results in a plethora of molecular changes, which are not always linked to histone acetylation, and that there is an essential need to understand the specific target(s) of any HDACi of interest. New lines of investigation are beginning to delve more deeply into target identification of specific HDACis and to address the relative toxicity of different HDACi classes. This review will focus on the utilization of HDACis during kidney organogenesis, injury, and disease, as well as on the development of these compounds as therapeutics.     

Roles of angiopoietins in kidney development and disease

Angiopoietins are a family of growth factors, the best studied being angiopoietin 1 (Ang-1), which binds to and tyrosine-phosphorylates endothelial Tie-2, causing enhanced survival and cell-cell stabilization. Ang-2 and Tie-1 downregulate Ang-1-induced Tie-2 signaling, and angiopoietin actions are further modified by vascular endothelial growth factor A and integrins. Metanephric capillaries express Tie genes, whereas metanephric mesenchyme, maturing tubules, and mature podocytes express Ang-1. Ang-1 null embryos begin to form blood vessels, but subsequent vascular remodeling fails, and analyses of chimeric wild-type/Tie null mutant embryos show that Tie genes are needed for renal endothelial survival. Ang-2 is transiently expressed in renal arterial smooth muscle and mesangial cells, and tubules around adult vasa rectae express Ang-2. Ang-2 null mice have increased pericytes around kidney cortical peritubular capillaries, perhaps an indirect consequence of upregulated Tie-2 signaling. Ang-1 therapies attenuate peritubular capillary loss in adult models of tubulointerstitial disease, although, in one study, this was accompanied by enhanced inflammation and fibrosis. Podocyte-directed Ang-2 transgenic overexpression causes glomerular endothelial apoptosis, downregulated nephrin expression, and increased albuminuria, and glomerular Ang-2 is upregulated in hyperglycemic and immune-mediated glomerulopathies. Thus, angiopoietins affect podocyte as well as glomerular endothelial biology, and imbalanced angiopoietin signaling contributes to glomerular pathobiology.     

Atubular glomeruli in a rat model of polycystic kidney disease

BACKGROUND: Autosomal-dominant polycystic kidney disease (ADPKD) is associated with a progressive decline in glomerular filtration rate (GFR) that often leads to end-stage renal disease. The basis for this decline in GFR is poorly understood. METHODS: Glomeruli in heterozygous Han:SPRD rats with ADPKD and their normal litter mates were studied by light microscopy, using serial sectioning techniques. The connections of the renal corpuscles to proximal tubules were classified as normal, atrophied, or absent (atubular glomerulus). Renal corpuscles also were examined by scanning electron microscopy. Single nephron glomerular blood flows were determined using microspheres. RESULTS: In the kidneys of six-month-old rats with ADPKD, 50% of the glomeruli were atubular and another 26% were associated with atrophied neck segments; these glomeruli were most often smaller in size than normal. About 16% of the glomeruli were hypertrophied and had normal connections to proximal tubules. Sclerotic changes in cystic kidney glomeruli were usually mild or moderate, and belied the failure of glomerular function. Glomerular blood flow in the cystic kidneys averaged half of normal and was markedly heterogeneous; the majority of small glomeruli displayed very low blood flows and a few showed relatively high blood flows. Fewer glomerular abnormalities were found in rats treated for five months with potassium citrate in their drinking water. CONCLUSIONS: The diminished GFR in the rat with ADPKD can be accounted for largely by the formation of atubular glomeruli. Compensatory glomerular hypertrophy also is present and may contribute to the progression of the renal disease.     

Histone deacetylases in kidney development: implications for disease and therapy

Histone deacetylases (HDACs) are an evolutionarily conserved group of enzymes that regulate a broad range of biological processes through removal of acetyl groups from histones as well as non-histone proteins. Recent studies using a variety of pharmacological inhibitors and genetic models of HDACs have revealed a central role of HDACs in control of kidney development. These findings provide new insights into the epigenetic mechanisms underlying congenital anomalies of the kidney and urinary tract (CAKUT) and implicate the potential of HDACs as therapeutic targets in kidney diseases, such as cystic kidney diseases and renal cell cancers. Determining the specific functions of individual HDAC members would be an important task of future research.     

类器官在肾脏疾病中的应用及研究进展

全球约有10%的成年人患有慢性肾脏疾病,不断攀升的肾脏疾病发病率对临床与公共卫生事业都是一个巨大的挑战。本文综述了近年来肾脏类器官的构建过程及其在肾脏疾病中的应用进展。类器官模型不仅在构建肾脏疾病模型中兼顾了动物模型和细胞培养的优点,还能对疾病进行治疗药物筛选和药物肾毒性检测。在未来,肾脏类器官也有望成为肾移植的供肾来...