大鼠肾小体发育中滤过屏障超微结构的演变

目的:探讨大鼠肾小体发育中滤过屏障超微结构的变化规律。方法:采用光镜、电镜技术,并结合体视学分析方法,对不同发育阶段大鼠滤过屏障超微结构的变化进行形态学观察和体视学测量。结果:在肾小体发育过程中,足细胞和内皮细胞的形状逐渐低平,内皮孔增多,足突及裂孔大量分化增多;足细胞下先出现电子密度较低的基膜,随后内皮细胞下才出现基膜,以后,二者融合形成一层电子密度较高的血管球基膜。结论:在大鼠肾小体的发育过程中,足细胞比内皮细胞先分泌基膜,然后二者融合形成血管球基膜。     

小鼠肾小体发育中的细胞形态学变化

目的：探讨小鼠肾小体发生和发育过程中各种细胞的形态变化。方法：应用组织培养、后肾移植和光、电镜技术对发育不同阶段的肾小体进行观察。结果：胚龄13d后肾尚未出现肾小体时,经培养5d,或移植到受鼠5d后出现了成熟的肾小体的结构。电镜下观察表明：上皮基膜先于内皮基膜出现,随后两层膜融合。早期内皮细胞无核部分是连续的,无小孔结构。在发育过程中,小孔结构增多。早期足细胞有两种类型,明型和暗型,细胞基部伸出小突起并穿过基膜与内皮细胞紧贴。结论：血管球来源于内源性后肾细胞。发育过程中足细胞与内皮有结构上的接触,上皮基膜先于内皮基膜出现,足细胞有两型。     

维生素E对慢性染镉肾小体滤过屏障超微结构损伤的保护作用

目的探讨维生素E(Vitamin E,VE)对慢性染镉小鼠肾小体滤过屏障超微结构损伤的保护作用。方法健康昆明种小鼠75只,体重28～32g,随机分3组:染镉组(CdCl 22mg/kg,皮下注射,每周2次,共3个月)、VE+镉组(染镉同时给VE 10mg/kg/天,灌胃)、正常对照组(注射等量生理盐水)。用透射电镜观察结合形态计量分析,研究经VE同时处理的慢性染镉小鼠肾小体滤过屏障的超微结构改变。结果染镉组肾小体滤过屏障的三层结构受损,与正常对照组相比,表现为毛细血管内皮增厚,血管系膜增生,血管球基膜增厚,基膜和内皮间有电子致密物沉积,足细胞次级突起间裂孔缩小和裂孔膜变薄等(P<0.001)。而VE+镉组滤过屏障的三层结构的上述变化明显减轻,形态接近正常(P>0.05)。结论VE可防止慢性染镉对肾小体滤过屏障的损害。     

小鼠肾小体发育中血管球毛细血管的分化

目的:探讨小鼠肾小体发育中血管球毛细血管内皮细胞的演变及毛细血管立体计量学的变化规律.方法:采用光镜、电镜技术,并结合体视学分析的方法,对不同发育阶段小鼠血管球毛细血管内皮细胞的演变及毛细血管立体计量学变化进行形态学观察和体视学测量.结果:在小鼠肾小体发育过程中,毛细血管内皮细胞的形状逐渐低平,内皮孔增多;从胚龄16 d到生后40 d,小鼠毛细血管的长度和表面积大约增大了64倍,体积大约增大了85倍.结论:在肾小体发育过程中,血管球毛细血管内皮孔的增多和血管球毛细血管的增大,为肾小体的滤过功能逐渐成熟提供了形态结构基础.     

大鼠肾小体发育中毛细血管形态的变化

目的:探讨大鼠肾小体发育中血管球毛细血管内皮细胞及毛细血管长度、表面积和体积的变化规律.方法:采用光镜、电镜技术,并结合体视学分析的方法,对不同发育阶段大鼠血管球毛细血管内皮细胞及毛细血管长度、表面积和体积的变化规律进行形态学观察和体视学测量.结果:在肾小体发育过程中,毛细血管内皮细胞由厚变薄,内皮孔从无到有,毛细血管袢逐渐增多;从胚龄18d到生后40d,毛细血管的长度和表面积大约增大了271倍,体积大约增大了110倍.结论:大鼠血管球毛细血管在肾小体滤过中起着重要作用.     

慢性镉中毒小鼠肾脏的超微结构观察

透射电镜下观察10只慢性镉中毒小鼠肾脏的超微结构变化，结果表明肾小体和近曲小管上皮细胞的超微结构均受损伤，肾小体，毛细血管内皮细胞肿胀，增厚，血管系膜增生，血管球基膜增厚或分裂成层，基膜和内皮细胞之间或基膜的分裂之间有电子致密物沉积，近曲小管上皮细胞，胞核变形，固缩，线粒体肿胀，嵴断裂，脱落，细胞游离面微绒毛肿胀，变形，排列紊乱，细胞基底面质膜内褶减少或消失，这些超微结构的改变与某些类型肾小球肾炎的病理特征相似。     

发育期小鼠肾小体细细胞增殖与凋亡的研究

目的研究小鼠肾小体发育过程中细胞增殖与凋亡的变化规律.方法采用PCNA免疫组织化学方法、末端脱氧核苷酸转移酶介导的缺口末端标记法（TUNEL染色法）和光、电镜技术,对发育不同阶段肾小体的细胞增殖和凋亡进行观察.结果 PCNA免疫组织化学染色显示：在Ⅰ和Ⅱ期肾小体内几乎所有细胞PCNA呈强阳性反应,Ⅲ、Ⅳ期肾小体PCNA阳性细胞数逐渐减少,Ⅴ期肾小体PCNA阳性细胞少见.TUNEL阳性细胞多出现在出生前,主要在Ⅲ、Ⅳ期肾小体表达.电镜观察：早期肾小体所有细胞核分裂象机率均高,Ⅲ期肾小体中的内皮细胞、足细胞核分裂象机率高,Ⅳ期肾小体中只见到内皮细胞核分裂象,Ⅴ期细胞核分裂象少见.电镜下所见的细胞凋亡多在Ⅲ、Ⅳ期肾小体,其中以内皮细胞、肾小囊壁层细胞凋亡居多.结论细胞增殖与凋亡行为在小鼠肾小体发育的整个过程中普遍存在,协同参与了调控肾小体正常发育过程.     

发育期小鼠肾小体细胞凋亡的研究

目的 研究小鼠肾小体发育过程中的细胞凋亡规律及形态学特点。方法 应用光镜、电镜技术和脱氧核糖核酸末端转移酶介导的dUTP缺口末端标记法(TUNEL法)分别对不同胚龄和生后日龄小鼠肾小体内细胞凋亡进行观察。结果 胚龄14d肾小体发生时就出现细胞凋亡，胚龄18d左右达到高峰，l随后缓慢下降。肾小体内凋亡细胞以内皮细胞和足细胞多见。凋亡细胞的两种结局：1．被邻近的细胞所吞噬；2．落人肾小体的毛细血管腔或肾小囊中。结论 小鼠肾小体的整个发育过程均存在细胞凋亡现象，肾小体内细胞凋亡与肾小体发育的完善有关。     

对胎儿肾脏的研究——Ⅰ.光镜及透射电镜的观察

本研究对14～28周5例胎儿肾脏的发生进行了光镜和透射电镜的观察。观察到肾单位的发生是由皮质深层向皮质浅层逐渐演化。皮质深层的肾小体较为成熟,形态结构与成年者相似。浅层为正在发育的原始肾小体。原始肾小体的毛细血管原基为间充质细胞团,在原始球囊的凹陷中逐渐分化成原始毛细血管,其内皮较厚,无孔亦无明显的基膜。较成熟的毛细血管才有明显完整的基膜。原始肾小体的足细胞为紧密排列的柱状细胞团,细胞之间有紧密连接和桥粒。此连接随细胞形态的改变而发生位置转移,并且是暂时的结构,当初级突和次级突形成后此连接相继消失。各肾小管的结构与所见文献报道相似。在28周胎儿肾脏中发现一未分化的肾小管,腔内有大量纤毛断面和脱落细胞碎片,其纤毛中微管排列为“7 1”、“6 1”及“5 1”不等。     

肾基膜来复红染色法的改良

肾小体的基膜位于足细胞与内皮的细胞之间,是由胶原蛋白和糖胺多糖组成的较厚的膜,是滤过屏障的主要组成部分,在生理机能上有着重要的意义.目前显示肾基膜有多种方法,在众多的染色法中,多数学者认为来复红染色法较简便,乐于接受,是较常见的显示肾基膜的一种方法,但其缺点是染色时间颇长,且药品不易得到,我们经多次实验观察,用醛品红代替来复红,获得了良好的效果,现将改良方法介绍如下.     

Structure of the amphibian mesonephric tubule during ontogenesis in Rana ridibunda L. tadpoles: early ontogenetic stages, renal corpuscle formation, neck segment and peritoneal funnels

The morphological changes produced in the mesonephric tubule during ontogenesis, not previously reported in amphibians, are described in Rana ridibunda tadpoles using light and electron microscopic methods. The rudimentary nephron units do not develop synchronously along the subperitoneal nephrogenic ridged cord. The first signs of morphogenesis are the presence of round euchromatinic nuclei and mitotic figures. The subsequent developmental stages are characterized by detachment of the rudimentary nephrons from the nephrogenic cord. Renal corpuscle formation is characterized by glomerular expansion, differentiation of large fenestrated capillaries and the presence of a discrete mesangium and a small capsular space. Interstitial capillaries next to the renal corpuscle rudiments appear to induce invagination and differentiation of the capsular epithelium. Developing podocytes were cuboidal undifferentiated epithelial cells with scarce primary processes and with an extensive part of the cell surface lying flat on the glomerular basement membrane. These features reflect low or no glomerular filtration during nephron development. The ciliated neck segment and peritoneal funnels show similar structural features. The latter were not physically connected with the nephrons, but opened into renal blood vessels. Involutive peritoneal funnels were observed.     

Structure of the amphibian mesonephric tubule during ontogenesis in Rana ridibunda L. tadpoles: early ontogenetic stages, renal corpuscle formation, neck segment and peritoneal funnels

The morphological changes produced in the mesonephric tubule during ontogenesis, not previously reported in amphibians, are described in Rana ridibunda tadpoles using light and electron microscopic methods. The rudimentary nephron units do not develop synchronously along the subperitoneal nephrogenic ridged cord. The first signs of morphogenesis are the presence of round euchromatinic nuclei and mitotic figures. The subsequent developmental stages are characterized by detachment of the rudimentary nephrons from the nephrogenic cord. Renal corpuscle formation is characterized by glomerular expansion, differentiation of large fenestrated capillaries and the presence of a discrete mesangium and a small capsular space. Interstitial capillaries next to the renal corpuscle rudiments appear to induce invagination and differentiation of the capsular epithelium. Developing podocytes were cuboidal undifferentiated epithelial cells with scarce primary processes and with an extensive part of the cell surface lying flat on the glomerular basement membrane. These features reflect low or no glomerular filtration during nephron development. The ciliated neck segment and peritoneal funnels show similar structural features. The latter were not physically connected with the nephrons, but opened into renal blood vessels. Involutive peritoneal funnels were observed.     

Lectin-binding sites during postnatal differentiation of normal and cystic rabbit renal corpuscles

Fluorochrome-labeled lectins were used to study the expression of glycoconjugates during the postnatal differentiation of normal and cystic rabbit renal corpuscles. Glomerular cysts (GC) are induced in the rabbit by a single injection of corticoids. The Bowman's capsule of these cysts is exclusively formed of podocytes (parietal podocytes). During normal development, the cell coat of the podocytes is intensely positive for wheat germ agglutinin (WGA) and Maclura pomifera agglutinin (MPA). This reaction decreases considerably during maturation, in parallel with an increase in the number of binding sites masked by terminal sialylation. Through-out the stages studied, the podocyte coat is peanut agglutinin (PNA)-negative, but it becomes intensely positive after neuraminidase treatment. Visceral and parietal podocytes in the glomerular cysts show the same pattern of glycosylation as the normal podocytes. In contrast, normal parietal cells only transiently expressed a weak reactivity to WGA and MPA during the first stages of differentiation, and did not express cryptic binding sites at any stage. The glomerular basement membrane (GBM) is positive to WGA, to succinylated WGA, and to MPA, in all the stages studied. Maturation of the GBM is characterized by expression of cryptic MPA-binding sites, and by a considerable increase in the number of cryptic PNA-binding sites. The basement membrane of the parietal layer of the cystic Bowman's capsule shows the same pattern of glycosylation, despite the fact that this epithelial layer is solely formed of podocytes and lacks endothelial cells. In contrast, the normal parietal basement membrane does not express PNA or MPA cryptic sites at any stage. On the whole, the only difference observed between normal and experimental kidneys is that the cysts show an advance in the temporal expression of glyconjugates with respect to the normal renal corpuscles. This suggests that the corticoids stimulate the terminal differentiation of the cellular components of the renal corpuscle.     

Ultrastructure of the renal corpuscle of the garter snake Thamnophis sirtalis

The renal corpuscle of the garter snake was examined using scanning and transmission electron microscopy, freeze-fracture and tracer experiments. The renal corpuscle was small and glomerular architecture simple. The visceral epithelium was composed of irregular, highly branched podocytes with broad, interdigitating foot processes. Numerous cell junctions, including fasciae occludentes and adhaerentes, occurred between podocytes. The podocytes bore numerous microvilli which projected into the urinary space and contained large bundles of microfilaments. The podocytes lay on a basal lamina which appeared to act as a primary filtration barrier.     

Nephrotoxicity of combined treatment with cisplatin and gentamicin in the guinea pig: glomerular injury findings

The drugs cisplatin and gentamicin are given consecutively to various cancer patients suffering from infections. Little information exists about the ultrastructural alterations of kidney glomeruli caused by treatment with these drugs. Renal glomeruli of guinea pigs treated with cisplatin alone and in combination with gentamicin were studied by transmission electron microscopy. The findings revealed foci of damage induced by cisplatin and especially by cisplatin/gentamicin in all glomerular components: glomerular capillaries, including their endothelial cells; basement membrane, epithelial podocytes, mesangial cells, and parietal cells of Bowman's capsule. The damage was expressed by endothelial cytoplasmic extrusions into the vascular lumen, thickening and lamination of capillary basement membrane, focal foot process fusion of podocytes, vacuolization in cytoplasm of endothelial cells of epithelial podocytes and of parietal cells, and the presence of lipid bodies and myeloid bodies in all glomerular cell types. Additionally, injurious effects to cytoplasmic organelles such as mitochondria, nuclei, and endoplasmic reticulum were observed. The results indicate that cisplatin alone and in combination with gentamicin is toxic to renal glomerular tissue. Since these drugs were previously found toxic for strial capillaries in the inner ear and since the main glomerular component is the glomerular capillaries, potential vascular damage and vascular complications in different body systems have to be taken into consideration when these drugs are needed in clinical use.     

Nephrotoxicity of Combined Treatment with Cisplatin and Gentamicin in the Guinea Pig: Glomerular Injury Findings

The drugs cisplatin and gentamicin are given consecutively to various cancer patients suffering from infections. Little information exists about the ultrastructural alterations of kidney glomeruli caused by treatment with these drugs. Renal glomeruli of guinea pigs treated with cisplatin alone and in combination with gentamicin were studied by transmission electron microscopy. The findings revealed foci of damage induced by cisplatin and especially by cisplatin/gentamicin in all glomerular components: glomerular capillaries, including their endothelial cells; basement membrane, epithelial podocytes, mesangial cells, and parietal cells of Bowman's capsule. The damage was expressed by endothelial cytoplasmic extrusions into the vascular lumen, thickening and lamination of capillary basement membrane, focal foot process fusion of podocytes, vacuolization in cytoplasm of endothelial cells of epithelial podocytes and of parietal cells, and the presence of lipid bodies and myeloid bodies in all glomerular cell types. Additionally, injurious effects to cytoplasmic organelles such as mitochondria, nuclei, and endoplasmic reticulum were observed. The results indicate that cisplatin alone and in combination with gentamicin is toxic to renal glomerular tissue. Since these drugs were previously found toxic for strial capillaries in the inner ear and since the main glomerular component is the glomerular capillaries, potential vascular damage and vascular complications in different body systems have to be taken into consideration when these drugs are needed in clinical use.     

Crescentic glomerulonephritis induced in the goat by immunization with homologous or heterologous glomerular basement membrane antigen.

Crescentic glomerular changes developed in goats 16 to 46 weeks after immunization with homologous or heterologous glomerular basement membrane (GBM) antigens incorporated in Freund's complete adjuvant. Mesangial widening, accumulation of migrant cells, fibrin deposition, and GBM thickening became manifest with time. The GBM was then attenuated and ruptured at a local area. Through the ruptured GBM, the influx of fibrin and blood cells occurred in the Bowman's space (BS) accompanying proliferation of epithelial cells lining the BS. The crescent thus formed was mainly composed of the capsular epithelial cells. The visceral epithelial cells (podocytes) and migrated blood cells contributed to the crescent formation to a lesser extent. Basement menbrane-like material appeared later between the crescentic cells and the crescent underwent a fibroepithelial form. The results indicate that the crescent develops in relation to the characteristic GBM damage with a resultant severe exudative change in the BS.     

CRESCENTIC GLOMERULONEPHRITIS INDUCED IN THE GOAT BY IMMUNIZATION WITH HOMOLOGOUS OR HETEROLOGOUS GLOMERULAR BASEMENT MEMBRANE ANTIGEN

Crescentic glomerular changes developed in goats 16 to 46 weeks after immunization with homologous or heterologous glomerular basement membrane (GBM) antigens incorported in Freund's complete adjuvant. Mesangial widening, accumulation of migrant cells, fibrin deposition, and GBM thickening became manifest with time. The GBM was then attenuated and ruptured at a local area. Through the ruptured GBM, the influx of fibrin and blood cells occurred in the Bowman's space (BS) accompanying proliferation of epithelial cells lining the BS. The crescent thus formed was mainly composed of the capsular epithelial cells. The visceral epithelial cells (podocytes) and migrated blood cells contributed to the crescent formation to a lesser extent. Basement menbrane-like material appeared later between the crescentic cells and the crescent underwent a Abroepithelial form. The results indicate that the crescent develops in relation to the characteristic GBM damage with a resultant severe exudative change in the BS.