CD36与肾间质泡沫细胞形成及血清胆固醇水平间的关系

我们既往的研究结果显示肾间质泡沫细胞的形成与蛋白尿的严重程度和血清胆固醇水平有关[1].Alport综合征患者血脂水平明显低于其他病理类型的肾小球疾病患者,但其泡沫细胞浸润的发生率却显著高于其他患者;另外膜增生性肾小球肾炎(MPGN)患者与局灶节段硬化性肾小球病(FSGS)患者相比两组间血清胆固醇水平差异无统计学意义,但两者泡沫细胞发生率却有显著差异[1].     

成人IgA肾病的临床与病理探讨

目的 回顾分析73例IgA肾病（IgAN）的临床表现与病理改变及其内在联系。方法 经常规肾穿刺活检获取年龄大于18岁的IgAN忠者的病理结果，并将临床表现及病理结果进行分类分型，同时获取IgAN的病理资料。结果 成人IgAN的临床表现以慢性肾炎为常见。占30例（41．1％）．其次是无症状血尿／尿检异常及肾病综合症。病理类型以系膜增生型肾小球肾炎常见，占39例（53．4%）。其次为局灶节段硬化性肾小球肾炎。慢性肾炎常见的病理类型为系膜增生性肾小球肾炎，其次为局灶节段硬化性肾小球肾炎和膜增殖性肾小球肾炎；无症状血尿／尿检异常及肾病综合症常见症理类为系膜增生型肾小球肾炎，其次为局灶节段硬化型肾小球肾炎；急性肾炎综合症以局灶节段增生性肾小球肾炎和系膜增生性肾小球肾炎为主，急进性肾炎主要表现为新月体肾炎．肾病综合征表现为系膜增生性肾小球肾炎和局灶节段硬化性肾小球肾炎。IgAN的病理特点以轻系膜增生为主，伴有部分及全球的硬化及间质的慢性化表现。结论 成人IgAN的临床表现以慢性肾炎最常见，病理类型以系膜增生性肾小球肾炎常见．慢性肾炎除局灶节段增生性肾小球肾炎外，其余各种病理类型均可以见到。急进性肾炎仅见于无症状性血尿／尿检异常，除新月体肾炎外。各种病理类型均可见到。IgAN的病理特点以轻系膜增生为主，同时中度及重度系膜增生占一定比例，并伴有肾小球硬化及间质纤维化，提示预后差，建议早期肾活检。积极干预治疗。     

成人肾小球微小病变的病理特征

目的探讨成人肾小球微小病变(minimal change disease,MCD)的临床病理学特点。方法回顾性分析符合肾病综合征(nephrotic syndrome,NS)、肾活检病理诊断为MCD、年龄≥18周岁的162例成人患者的病理特征。结果对162例成人MCD肾组织病理改变进行统计发现,肾小球球性硬化、肾间质纤维化、肾间质炎细胞浸润、肾小管萎缩、肾血管病变的比率分别为32.7%、42.6%、55.6%、45.7%、37.0%,除肾间质炎细胞浸润,余病理改变的比率均随着年龄的增长而增加。经年龄纠正后,肾小球球性硬化的比率与患者年龄的关联消失。结论成人MCD病理改变随年龄增长,病变比例及严重程度均增高。     

DC细胞和过渡性B细胞水平与IgA肾病患者病理分型及患者预后不良的关系

目的探讨过渡性B淋巴细胞、树突细胞(dendritic cells, DCs)水平与IgA肾病(IgA nephropathy,IgAN)患者病理分型的关系及对患者预后不良的预测价值。方法选取2012年1月至2016年1月我院收治的85例IgAN患者以及同期108例健康体检者作为研究对象。采用免疫荧光法检测肾组织DC数目和分布情况,采用流式细胞仪检测外周静脉血中CD19+CD27-CD38hi细胞水平,对IgAN患者进行肾脏组织病理分型,并分析DC细胞和过渡性B细胞与临床病理指标及预后之间的关系。结果研究组IgAN患者肾小球和肾小管间质组织中的CD209细胞水平高于健康对照组,外周血中CD19+CD27-CD38hi占B淋巴细胞百分率低于对照组(P<0.05)。肾小球、肾小管间质的DC数目、免疫荧光DC水平与牛津病理分型具有相关性(P<0.05)。Spearman相关分析显示,肾小管间质中DC数目与肾小管间质纤维化比例、肾小球硬化比例之间存在显著正相关性(P<0.05),CD19+CD27-CD38hi细胞比例与血尿素氮、血肌酐、尿蛋白量、肾小球硬化比例、节段性硬化比...     

M型磷脂酶A2受体及其抗体和Nephrin在不同类型膜性肾病患者的表达

目的:检测不同类型膜性肾病(membranous nephropathy,MN)患者肾组织PLA2R、Nephrin及血清anti-PLA2R的表达量,判断它们之间是否存在相关性及其意义。方法:收集MN患者37例为实验组,包括特发性膜性肾病(idiopathic membranous nephropathy,IMN)患者23例、HBV相关性MN(HBV-MN)患者8例、V型狼疮性肾炎(stage V lupus nephritis,LN-V)患者6例,选取10例肾肿瘤行一侧肾切术患者为对照组。应用免疫组织化学法检测各组肾组织中PLA2R及Nephrin的表达,通过专业图像处理软件对其表达进行半定量分析,并应用ELISA检测各组血清anti-PLA2R的表达量。结果:1)各实验组及对照组均可见PLA2R及Nephrin沿肾小球毛细血管袢沉积。IMN组PLA2R较其余各组表达量明显升高,差异有统计学意义,而剩余三组比较无统计学差异。各组Nephrin相对表达量,对照组>LN-V>HBV-MN>IMN,差异有统计学意义;2)IMN组肾组织Nephrin相对表达量同肾组织PLA2R及血清anti-PLA2R浓度间均负相关,肾组织PLA2R相对表达量同血清anti-PLA2R浓度呈正相关;3)IMN组中血清anti-PLA2R阳性者其肾组织PLA2R均表达升高。结论:IMN患者肾组织中PLA2R的表达较继发性膜性肾病(secondary membranous nephropathy,SMN)及正常对照组高,IMN组中血清anti-PL A2R阳性者其肾组织PL A2R均表达升高,临床上可联合二者共同鉴别MN是否原发,结合肾组织中Nephrin的检测,可增强其敏感性。PLA2R同足细胞裂孔隔膜蛋白Nephrin于IMN患者肾组织表达量呈负相关,为IMN的发病机制的研究提供进一步支持。     

Expression of CD2AP on podocytes with different pathological types of nephrotic syndrome

目的 观察不同病理类型的原发性肾病综合征(nephrotic syndrome,NS)患者肾小球足细胞中CD2相关蛋白(CD2AP)的表达,探讨其与足细胞损伤的关系.方法 选取原发性NS患者54例,10例同期肾肿瘤切除患者正常肾组织作为对照.肾活检后常规染色观察肾脏组织病理改变,肾组织行免疫荧光法CD2AP和肾小球上皮细胞蛋白-1(GLEPP1)双重标记,对肾小球CD2AP的表达进行定位;分别用real time PCR和免疫组化SP法检测组织中CD2AP的表达,采用real time PCR检测nephrin的表达,透射电镜观察足细胞的结构变化,并定量测量足突密度.结果 (1)NS患者肾小球中CD2AP的表达及nephrin的表达下调,足细胞足突不同程度融合,足突密度降低.(2)病理表现为微小病变性肾病(minimal change disease,MCD)、局灶性节段性肾小球硬化(focal segmental glomerulosclerosis,FSGS)和膜性肾病(membranous nephropathy,MN)的NS患者CD2AP表达及nephrin表达较对照组明显降低,且CD2AP与nephrin表达呈正相关,病理表现为MCD和FSGS的NS患者CD2AP表达与足突密度呈正相关.结论 本研究首次发现原发性NS患者肾小球足细胞中CD2AP的表达降低,且在MCD和FSGS中与足细胞病变程度相关,提示CD2AP低表达在足细胞病变为主的肾小球疾病中发挥重要作用.CD2AP有利于诊断足细胞病变的早期检测,对CD2AP表达减低进行早期干预可能有助于延缓疾病进展.     

特发性膜性肾病相关基因单核苷酸多态性研究进展

<正>膜性肾病是成人肾病综合征的主要病理表现之一,特征性的病理学改变是肾小球毛细血管袢上皮侧出现大量免疫复合物沉积。典型临床表现为大量蛋白尿、低蛋白血症、高脂血症和水肿等。膜性肾病按照病因可分为特发性膜性肾病(Idiopathic membranous nephropathy,IMN)和继发性膜性肾病(Secondary membranous nephropathy,SMN)。IMN的发病     

小儿局灶节段性肾小球硬化53例临床病理分析

目的：探讨小儿局灶节段性肾小球硬化（FSGS）的病理特点及发病机制。方法：对53例肾穿标本进行光镜，电镜及免疫荧光检测，结果：肾小球局灶节段性透明变性及间质泡沫细胞浸润在小儿原发性FSGS中是一个较为特性的表现。原发性FSGS中，尖端病变一型预后良好，一部分轻微病变患者可能发展为FSGS。出现继发性FSGS则是预后不良的表示。结论：区别原发性还是继发性FSGS对临床治疗，估计预后意义重大。     

CD2相关蛋白在肾病综合征中的表达及意义

目的观察不同病理类型的原发性肾病综合征(nephrotic syndrome,NS)患者肾小球足细胞中CD2相关蛋白(CD2AP)的表达,探讨其与足细胞损伤的关系。方法选取原发性NS患者54例,10例同期肾肿瘤切除患者正常肾组织作为对照。肾活检后常规染色观察肾脏组织病理改变,肾组织行免疫荧光法CD2AP和肾小球上皮细胞蛋白-1(GLEPP1)双重标记,对肾小球CD2AP的表达进行定位;分别用real time PCR和免疫组化SP法检测组织中CD2AP的表达,采用real time PCR检测nephrin的表达,透射电镜观察足细胞的结构变化,并定量测量足突密度。结果 (1)NS患者肾小球中CD2AP的表达及nephrin的表达下调,足细胞足突不同程度融合,足突密度降低。(2)病理表现为微小病变性肾病(minimal change disease,MCD)、局灶性节段性肾小球硬化(focal segmental glomerulosclerosis,FSGS)和膜性肾病(membranous nephropathy,MN)的NS患者CD2AP表达及nephrin表达较对照组明显降低,且CD2AP与nephrin表达呈正相关,病理表现为MCD和FSGS的NS患者CD2AP表达与足突密度呈正相关。结论本研究首次发现原发性NS患者肾小球足细胞中CD2AP的表达降低,且在MCD和FSGS中与足细胞病变程度相关,提示CD2AP低表达在足细胞病变为主的肾小球疾病中发挥重要作用。CD2AP有利于诊断足细胞病变的早期检测,对CD2AP表达减低进行早期干预可能有助于延缓疾病进展。     

277例肾病患者足细胞相关分析

目的 分析肾脏疾病患者不同类型的病理改变与足细胞数量的关系,研究二者之间的相关性,寻找足细胞在判断疗效与预后方面的积极意义.方法 对277例肾穿病人肾组织进行常规病理染色及免疫荧光、电镜检查进行病理分型,同时进行肾脏足细胞计数,对二者进行相关性分析,了解肾小球足细胞数量与肾脏病病理分型及预后是否相关.结果 局灶节段性肾小球肾炎(FSGS)、膜性肾病(MN)与搪尿病肾病(DN)和足细胞病变有绝对关系:肾小球足细胞数目与尿蛋白多少呈负相关;尿蛋白是临床判断肾脏病活动与否的依据之一.结论 故肾小球足细胞可以作为判断临床肾病活动的依据之一.     

Renal expression of intercellular adhesion molecule-1 in immunoglobulin A nephropathy: tubulointerstitial injury and prognosis

In immunoglobulin A nephropathy (IgAN), the abnormal expression of intercellular adhesion molecule-1 (ICAM-1) on proximal tubule epithelium is associated with the glomerular and interstitial infiltration of leucocytes, but its clinical significance remains uncertain. We analysed the relationship between the ICAM-1 (CD54) expression in tubular epithelial cells and interstitial leucocytes, macrophages (CD14) and T lymphocytes (CD3) with the histologic features, proteinuria and serum creatinine at the time of renal biopsy and after 2.42 years in 45 patients with IgAN and after 1.8+/-1.5 years in 29 patients with non-glomerulonephritis (non-GN). In IgAN, ICAM-1+ tubule epithelium was 0.1+/-0.18 (x+/-SD), and this was associated with extracapillary proliferation (up to 20% of Bowman's space), glomerular sclerosis involving less than 50% of glomerular area, interstitial cellular infiltration, tubular atrophy and proteinuria level. ICAM-1+ interstitial leucocytes were correlated with glomerular sclerosis involving less than 50% of glomerular area, glomerular sclerosis involving more than 50% of glomerular area, tubular atrophy, interstitial fibrosis and serum creatinine level. In patients with an increase of 50% in serum creatinine, ICAM-1+, CD14+ and CD3+, interstitial leucocytes were significantly outnumbered than in patients with stable serum creatinine. In non-GN, ICAM-1+ tubule epithelium was 0.02+/-0.04 (U=344, P<0.05, vs IgAN), and this was inversely correlated with the percentage of the normal glomeruli and associated with glomerular sclerosis covering more than 50% of glomerular area, tubular atrophy and serum creatinine level. The association between tubular ICAM-1 and proteinuria and the association between interstitial ICAM-1+, CD14+ and CD3+, leucocytes and renal failure at presentation and the deterioration in IgAN in contrast with non-GN suggest that tubular and interstitial expression of ICAM-1 may be a marker of tubulointerstitial disturbance in IgAN.     

Podocyte Injury–Driven Lipid Peroxidation Accelerates the Infiltration of Glomerular Foam Cells in Focal Segmental Glomerulosclerosis

Intracapillary foam cell infiltration with podocyte alterations is a characteristic pathology of focal segmental glomerulosclerosis (FSGS). We investigated the possible role of podocyte injury in glomerular macrophage and foam cell infiltration in a podocyte-selective injury model (NEP25 mice) and hypercholesterolemic model [low-density lipoprotein receptor deficiency (LDLR^−/−) mice] with doxorubicin–induced nephropathy. Acute podocyte selective injury alone failed to induce glomerular macrophages in the NEP25 mice. However, in the doxorubicin-treated hypercholesterolemic LDLR^−/− mice, glomerular macrophages/foam cells significantly increased and were accompanied by lipid deposition and the formation and ingestion of oxidized phospholipids (oxPLs). Glomerular macrophages significantly correlated with the amount of glomerular oxPL. The NEP25/LDLR^−/− mice exhibited severe hypercholesterolemia, glomerular lipid deposition, and renal dysfunction. Imaging mass spectrometry revealed that a major component of oxidized low-density lipoprotein, lysophosphatidylcholine 16:0 and 18:0, was present only in the glomeruli of NEP25/LDLR^−/− mice. Lysophosphatidylcholine 16:0 stimulated mesangial cells and macrophages, and lysophosphatidylcholine 18:0 stimulated glomerular endothelial cells to express adhesion molecules and chemokines, promoting macrophage adhesion and migration in vitro. In human FSGS, glomerular macrophage–derived foam cells contained oxPLs accompanied by the expression of chemokines in the tuft. In conclusion, glomerular lipid modification represents a novel pathology by podocyte injury, promoting FSGS. Podocyte injury–driven lysophosphatidylcholine de novo accelerated glomerular macrophage–derived foam cell infiltration via lysophosphatidylcholine–mediated expression of adhesion molecules and chemokines in glomerular resident cells.Focal segmental glomerulosclerosis (FSGS) is a progressive kidney disease caused by podocyte injury.^1–4 The pathology of FSGS includes a variety of glomerular features. The Columbia classification system divides FSGS into the following five variants: not otherwise specified, perihilar variant, cellular variant, tip variant, and collapsing variant.^1,5,6 The classification is useful for predicting the prognosis in FSGS.^1,5–7Glomerulosclerosis is defined by its pathological characteristics, including capillary collapse accompanied by deposition of extracellular matrices and/or hyaline materials. This classic feature of sclerosis is usually observed in not otherwise specified and perihilar variants, whereas it is not observed in the definition of other variants. To diagnose FSGS in the absence of classic sclerosis, the infiltration of foam cells in the glomerular segment is a good marker, particularly in cellular variants.^1,7 Although glomerular foam cells can be observed in any variant of FSGS and are thought to be involved in disease progression, the mechanism underlying foam cell infiltration in FSGS remains largely unknown.Studies have shown that glomerular foam cells were associated with extremely high levels of serum lipids in patients with familial hypercholesterolemia and lecithin-cholesterol acyltransferase deficiency.^8,9 Glomerular foam cells were also observed in experimental models of hypercholesterolemia,^10–15 suggesting that high levels of serum lipids may be a plausible basis for glomerular foam cell infiltration. Some studies reported that glomerular foam cells were associated with nephrotic syndrome in humans, including membranous glomerulonephritis, diabetic nephropathy, and IgA glomerulonephritis.^16–18 However, in these cases, the glomerular foam cells were not always associated with hyperlipidemia. A previous study demonstrated that glomerular foam cells were not correlated with serum cholesterol levels in FSGS patients.⁷ Likewise, glomerular foam cells were absent in minimal change disease, despite the presence of similar levels of serum lipids observed in FSGS.¹⁹ These findings suggest that additional factors other than serum lipid levels may account for the formation of glomerular foam cells in FSGS.The characteristic histology of glomerular foam cell formation in FSGS is its segmental and intracapillary localization associated with overlaying podocyte abnormalities. Because podocyte injury represents the common basis of FSGS, there may be a causal relationship between podocyte injury and foam cell accumulation in particular variants of FSGS.Most glomerular foam cells are derived from CD68-positive macrophages,^20,21 which transform into foam cells by ingesting lipids within the glomerulus in situ. As demonstrated in the mechanism of atherosclerosis, it seems that the development of glomerular foam cell infiltration in FSGS is because of the interaction and catenation of several factors, including the extent and duration of hyperlipidemia, lipid characteristics, and the response of glomerular resident cells.^22–24The present study assessed the stepwise development of glomerular foam cell infiltration using transgenic murine models of FSGS, with podocyte-specific injury and hypercholesterolemia caused by low-density lipoprotein receptor (LDLR) deficiency. We performed imaging mass spectrometry (IMS) analysis to determine the biochemical characteristics of glomerular lipid peroxidation and conducted an in vitro study to assess changes in the molecular profiles of mesangial cells and endothelial cells in response to podocyte injury–driven lipid modifications. Our results suggest that podocyte injury promotes hypercholesterolemia-based lipid deposition and specific peroxidation, which activate a molecular network within a glomerular microenvironment that induces macrophage recruitment and foam cell formation in FSGS.     

AITD合并肾小球肾炎自身抗体检测及临床病理分析

目的：观察自身免疫性甲状腺疾病合并肾小球肾炎的甲状腺自身抗体表达及临床病理特点。方法：自1998年～2007年行肾活检的肾小球肾炎合并AITD患者20例,分析其甲状腺自身抗体表达及临床与病理特点。结果：AITD 20例（男6,女14）,平均年龄（35.7±9.4）岁,Graves’病9例,桥本氏甲状腺炎5例,甲减6例。甲状腺球蛋白抗体（TGA）、甲状腺微粒体抗体（TMA）、甲状腺过氧化物酶抗体（TPO-Ab）三种自身抗体中,TPO-Ab阳性率较高。肾损害表现为隐匿性肾炎3例,慢性肾小球肾炎8例,肾病综合征6例,急进性肾炎3例。病理提示膜性肾病9例,4例为系膜增生性肾小球肾炎,3例为坏死性肾小球肾炎,2例为局灶节段硬化,2例为系膜毛细血管性肾炎。结论：自身免疫性甲状腺疾病合并肾小球肾炎肾损害主要表现为慢性肾炎和肾病综合征,肾脏病理类型多为膜性肾病,TPO-Ab阳性率较高。大多数患者预后较好。     

An analysis of 4,514 cases of renal biopsy in Korea

To evaluate the distribution and changing patterns of renal diseases in Korea, a total of 4,514 cases of renal biopsy collected over a 23-year period between 1973 and 1995 were reviewed. Of 4,200 cases excluding 314 unsatisfactory biopsies, adult cases comprised 59.5% and pediatric cases, 40.5%. The male to female ratio was 1.5:1 in adults and 2.2:1 in children. Glomerulonephritis (GN) comprised 80.0% of the total. The most common primary GN in adults was minimal change disease (MCD) (26.6%), followed by IgA nephropathy (IgAN) (22.1%), membranous GN (MGN) (11.8%), and membranoproliferative GN (MPGN) (5.9%). In children, the primary GN incidence rates were MCD (24.8%), IgAN (10.3%), poststreptococcal (including postinfectious) GN (PSGN) (8.6%), and focal segmental glomerulosclerosis (FSGS) (4.0%). The most common secondary GN in adults was lupus nephritis and in children Henoch-Schonlein purpura nephritis. The most common cause of nephrotic syndrome was MCD in both adults and children, followed by MGN and FSGS. The elderly, aged sixty years and older, comprised 2.7% of cases and recorded equal numbers of MCD and MGN. The proportion of the biopsies found to be seropositive for HBs antigen was 27.9%, and these showed either MGN or MPGN pattern. Repeat biopsy was performed in 168 patients, due to previous biopsy failure in 15.5%. When the primary GN cases were analyzed at 5-year intervals, the prevalence of PSGN, which was greater than 25% during the 1973-1982 period, decreased abruptly in children thereafter, whereas the prevalence of FSGS increased slowly since the 1988-1992 period in both adults and children. The decrease of PSGN and the increase of FSGS suggest a role for socioeconomic and environmental factors in Korea.     

IgA肾病患者血清肽谱的差异性研究

目的 研究IgA肾病患者血清肽谱的差异性,筛选IgA肾病早期诊断的生物标记.方法 选取解放军第一八一医院肾脏科2008年8月至2009年3月就诊的患者或体检的健康人为研究对象,分为试验组和对照组,试验组为33例IgA肾病患者,对照组为10例健康志愿者、12例微小病变、10例局灶硬化和10例膜性肾病患者.ClinProt系统下采用磁珠浓缩和基质辅助激光解吸电离-飞行时间-质谱技术分析IgA肾病组与其他各组研究对象血清肽谱的差异.结果 分别筛选出5个、5个、3个、3个差异性多肽作为诊断IgA肾病与健康者、微小病变、局灶硬化、膜性肾病的潜在生物标记.结论 应用蛋白质组学技术成功建立了IgA肾病患者血清肽谱的诊断模型,为蛋白质组学技术用于IgA肾病的早期诊断提供了新的思路.     

Renal tubular basement membrane changes in tubulointerstitial damage in patients with glomerular diseases

Injury to renal tubules and interstitium occur in various glomerular diseases, leading to functional impairment. Tubular basement membrane (TBM) is an important component in maintaining tubular epithelial cell integrity. Because ultrastructural changes in these structures had not been studied in detail, the authors analyzed 30 patients with various types of glomerular diseases, including minimal change disease (MCD), focal segmental glomerular sclerosis, IgA nephropathy, diffuse proliferative glomerulonephritis, membranous nephropathy, and lupus nephritis, by light, electron, and immunofluorescence microscopy. Ultrastructural changes in the TBM were studied and morphometric measurements were performed. The tubular basement membranes showed membranous structures, lucent or lytic areas, and tubular epithelial detachment. There was significant linear correlation between these tubular basement membrane changes and terminal complement complex neoantigens. The interstitial widening was due to banded collagen fibers, with anchoring fibers in the TBM. The various glomerular diseases lead to tubulointerstitial damage via changes in the TBM, leading to renal dysfunction.     

用PCR-SSO检测IgA肾炎HLA-DRB1、DQA1、DQB1等位基因及其临床意义

利用聚合酶链区应（PCR）和序列特异性寡核苷酸（SSO）探针技术对47例经临床及免疫荧光证实的IgA肾病（IgAN）患者HLA-DRB1、DQA1、DQB1等位基因频率进行了检测。结果显示IgAN患者组DR4基因频率明显高于正常人组,相反DQB1*0602基因频率与对照组相比呈显著下降。IgAN患者中蛋白尿组DR4基因频率显著高于对照组,而肉眼血尿组与对照组无显著差异。约 1/4 DR4基因阳性的IgAN病理表现为局灶节段硬化性肾小球肾炎。 IgAN肾衰组DR4阳性的发生率显著高于非肾衰组。由此可见,IgAN中HLA-DR4基因频率而著增高, DR4阳性IgAN临床多表现蛋白尿,易发生肾衰,病理多呈局灶节段硬化型;DQB1*0602等位基因对IgAN可能有一定抵抗性。这些研究结果提示IgAN有免疫遗传的背景。     

Renal Tubular Basement Membrane Changes in Tubulointerstitial Damage in Patients with Glomerular Diseases

Injury to renal tubules and interstitium occur in various glomerular diseases, leading to functional impairment. Tubular basement membrane (TBM) is an important component in maintaining tubular epithelial cell integrity. Because ultrastructural changes in these structures had not been studied in detail, the authors analyzed 30 patients with various types of glomerular diseases, including minimal change disease (MCD), focal segmental glomerular sclerosis, IgA nephropathy, diffuse proliferative glomerulonephritis, membranous nephropathy, and lupus nephritis, by light, electron, and immunofluorescence microscopy. Ultrastructural changes in the TBM were studied and morphometric measurements were performed. The tubular basement membranes showed membranous structures, lucent or lytic areas, and tubular epithelial detachment. There was significant linear correlation between these tubular basement membrane changes and terminal complement complex neoantigens. The interstitial widening was due to banded collagen fibers, with anchoring fibers in the TBM. The various glomerular diseases lead to tubulointerstitial damage via changes in the TBM, leading to renal dysfunction.     

Prognostic significance of glomerular and tubulointerstitial morphometry in idiopathic membranous nephropathy

The purpose of our study was to investigate the prognostic value of clinical and pathological, in particular glomerular and tubulointerstitial morphometric variables in idiopathic membranous nephropathy (IMN). We prospectively followed 60 Caucasian patients diagnosed with idiopathic membranous nephropathy for at least 2 years or until primary outcome (≥50% permanent decrease in estimated glomerular filtration rate or death). Glomerular and tubulointerstitial morphometric variables at the time of renal biopsy were analyzed with respect to this outcome. Univariate analysis revealed that significant negative prognostic factors for this outcome were higher cholesterol and smaller albumin concentrations, higher creatinine and maximal 24-h proteinuria, higher grade of nephroangiosclerosis, higher glomerular basement membrane thickness and glomerulopathy index, higher interstitial fibrosis and tubular atrophy percentage and higher injury score. In multivariate analysis, only the maximal 24-h proteinuria and interstitial fibrosis and tubular atrophy percentage were independent predictors of this outcome. The results suggest that morphometric analysis, mainly quantitative measurement of interstitial fibrosis and tubular atrophy percentage, injury score, glomerular basement membrane thickness and glomerulopathy index could be used as an additional method for risk stratification of patients with idiopathic membranous nephropathy.     

An analysis of 2361 cases of renal biopsy in Korea

To evaluate the distribution pattern of renal diseases based on needle biopsy, we analyzed 2361 cases of renal biopsy and necropsy material examined at the Department of Pathology from 1973 to 1988. The average age was 21.1 years for males and 23.7 years for females. The adult cases comprised 60.2% and the child cases 39.8%. The male to female ratio was 1.6: 1 in adults and 2.3:1 in children. Glomerular diseases were 97.8% of the total; primary glomerulonephritis (GN) 59.8% and secondary GN 27.6% The major glomerular diseases, in descending order of frequency, were; minimal change nephrotic syndrome (MCNS; 24.2%), IgA nephropathy (IgAN; 17.8%), benign recurrent hematuria (BRH; 8.8%), membranous GN (MGN; 7.9%), acute poststreptococcal GN (APSGN; 7.3%), mesangioproliferative GN (MspGN; 5.5%), minimal mesangiopathy (5.5%), membranoproliferative GN(4.1%), and focal segmental glomerulosclerosis (FSGS; 2.7%). GN of systemic disease included 77 cases of lupus nephritis, 157 cases of Henoch-Sch?nlein purpura nephritis (HSPN) and 7 cases of systemic infection excluding Hepatitis B viral hepatitis. The most common glomerular diseases were MCNS, IgAN, MGN and MspGN in adults, and MCNS, BRH, HSP-N and APSGN in children. HBs antigenemia was found in 71 cases, of which MGN and IgAN were the most frequent. HBs antigenemia-associated MGN was prevalent in male children, whereas IgAN was prevalent in adults.(ABSTRACT TRUNCATED AT 250 WORDS)