阿霉素肾病肾小球硬化动物模型的研究

目的:探讨肾小球硬化不同病理发展阶段动物模型的制作.方法:采用单侧肾切除并高低剂量阿霉素尾静脉注射法建立大鼠肾小球硬化模型,观察各组大鼠血尿生化和肾组织病理改变.结果:8周时高低剂量阿霉素模型组均出现尿蛋白排出增加,血脂升高,肾功能下降;高剂量阿霉素注射组光镜下肾小球硬化达80%以上,呈弥漫性,其中25%～50%呈球性硬化,肾小球脏层上皮细胞足突广泛融合或消失;肾小管病变严重,肾小管上皮细胞肿胀、颗粒变性、坏死甚至脱落入小管腔,可见大量蛋白管型;间质纤维化和大量炎细胞浸润;低剂量阿霉素注射组肾小球硬化呈局灶节段性分布,肾小球肥大,肾小囊扩张,约50%肾小球有不同程度的硬化,球性硬化达10%左右,间质可见明显纤维化和局灶性炎细胞.结论:阿霉素对肾小球脏层上皮细胞、毛细血管内皮细胞及肾小管上皮细胞均有明显毒性损伤;高低剂量阿霉素注射组均为病变稳定的肾小球硬化模型,其中高剂量阿霉素注射组肾小球硬化模型为中晚期病理改变;低剂量阿霉素注射组为肾小球硬化早期病理改变.     

二维平面足细胞相对密度测量法

目的：探索一种简便且临床实用的足细胞丢失评估方法。方法：应用免疫组化法对正常和阿霉素肾病大鼠的肾组织,以及正常肾组织和3种不同病理类型肾小球疾病患者肾组织进行Wilms′瘤蛋白免疫染色,采用手工计数和病理图像分析技术相结合的方法分别对单个肾小球内足细胞的绝对数以及单位面积肾小球内足细胞的相对密度进行测定,找出结果可靠的最低肾小球数目并检验不同测量人员所获结果的一致性。结果：在统计10个和15个大鼠肾小球时,阿霉素肾病组肾小球足细胞相对密度显著低于正常大鼠;无论统计的肾小球数目多少,两组大鼠肾小球足细胞绝对数差异无统计学意义。在统计5个和10个人类肾小球时,局灶节段性肾小球硬化组和膜性肾病组肾小球足细胞相对密度均显著低于正常组和微小病变组;局灶节段性肾小球硬化组肾小球足细胞绝对数显著低于正常组和微小病变组。人类肾小球足细胞相对密度与血肌酐（Scr）水平呈低度负相关,但与24h尿蛋白含量（24hUPQ）无相关关系;阿霉素肾病大鼠肾小球足细胞相对密度与Scr、24hUPQ无相关关系。两名检测者所获结果有高度一致性。结论：这种足细胞相对密度评估法简便、快捷和可靠,且所需肾小球数目少,有望在临床实践中推广。     

阿霉素肾病动物模型的国外研究进展

阿霉素。肾病动物模型于20世纪80年代初期由国外文献报道，是目前公认的能较好模拟人类慢性肾脏病的动物模型，在肾脏病研究领域已广泛应用。根据其建立方法和病理表现，可分为急性模型和慢性模型，急性模型类似于人类微小病变型肾病（MCN），而慢性模型类似于人类局灶节段性肾小球硬化（FSGS）。阿霉素肾病动物模型的建立与所选动物品系，     

阿霉素注射次数及剂量对肾病综合征模型的影响

目的：建立阿霉素（ADR）大鼠肾病综合征模型,探讨相关影响因素,考察阿霉素的给药剂量与造模方法（一次性注射和分次注射）,确立造模的最佳条件。方法：利用尾静脉一次性注射和分次注射阿霉素,构建大鼠肾病综合征动物模型。结果：阿霉素造模后大部分出现尿蛋白排出量增加、精神不佳等现象。B组（一次性尾静脉注射ADR7.5mg/kg）死亡率66.7%,C组（分二次尾静脉注射ADR,共7.5mg/kg）,D组（一次性尾静脉注射ADR6mg/kg）死亡率25%;F组（一次性尾静脉注射ADR5mg/kg）,尿蛋白含量相对于其他几组偏低;E组（分二次尾静脉注射ADR,共6mg/kg）大鼠精神状态良好,能较快时间达到较高的尿蛋白含量（〉250mg/24h）;病理切片显示E组出现肾小球局灶节段性硬化和节段性纤维素样坏死。结论：从精神状态、尿蛋白含量、死亡率、病理切片等综合比较,尾静脉注射ADR4mg/kg,1周后再注射2mg/kg,4周后可以高效地复制出阿霉素肾病综合征大鼠模型。     

阿霉素肾病大鼠药理应用实验研究进展

Wistar或SD大鼠静脉注射阿霉素造成的急性模型类似微小病变性肾病综合征 (NS) :光镜下病变甚微 ;电镜下肾小球上皮细胞足突肿胀、融合。处理鼠一般于用药后 4～6d出现蛋白尿 ,13～ 15d出现大量蛋白尿 ,30d左右出现显著低蛋白血症、高脂血症和明显水肿[1] ,目前已广泛应用于NS的各种实验研究。本文就阿霉素肾病 (AN)大鼠在国内NS药理应用研究方面的进展作一概述。　　 1　抗氧化剂AN鼠的发病机理与氧自由基 (OFR)产生、脂质过氧化物 (LPO)形成 ,对肾小球和肾小球上皮细胞产生毒性 ,造成肾小球滤过膜电荷屏障缺损和对分子控制的缺乏 ,…     

霉酚酸酯对局灶节段性肾小球硬化大鼠肾脏的保护作用

目的观察霉酚酸酯对局灶节段性肾小球硬化大鼠残肾的保护作用。方法给予局灶节段性肾小球硬化大鼠霉酚酸酯（MMF）50mg·kg^-1·d^-1、雷公藤20mg·kg^-1·d^-1。8周后观察大鼠24h尿蛋白定量、血尿素氮（BUN）、血肌酐（SCr）、血浆白蛋白（Alb）的含量以及肾脏病理改变。结果两药均能减少尿蛋白,降低BUN。在肾脏病理上,局灶节段性肾小球硬化大鼠出现局灶性肾间质纤维化,肾小球硬化,用药后病变减轻,以MMF减轻更为显著。结论MMF能抑制局灶节段性肾小球硬化大鼠肾脏中细胞的异常增殖,减少间质纤维化及肾小球硬化,减少蛋白尿,减轻肾脏的损害。     

局灶节段性肾小球硬化的新病理分型

局灶节段性肾小球硬化(FSGS)由Rich在1957年首先描述,其发生率有逐年增高趋势.FSGS是一种临床病理综合征,其特点为蛋白尿,常为肾病性蛋白尿,同时伴局灶节段性肾小球硬化和足突的消失.疾病早期,仅部分肾小球(＜50%)和/或部分毛细血管襻(<50%)发生硬化性改变.随着病变进展,肾小球逐渐弥漫硬化,甚至出现球性硬化.     

叶任高教授治疗常复发性肾病综合征的经验

常复发性肾病综合征（PNS）是指经激素治疗后能完全缓解,但在半年内复发2次或一年之内复发3次以上者。肾病综合征反复发作,可以使肾小球病理损害进一步加重,从微小病变型转变为局灶节段硬化型,乃至肾小球硬化,最终出现终末期肾衰竭,故及早有效的治疗十分重要。     

局灶节段性肾小球硬化症大鼠尿足细胞动态检测及其意义

目的建立局灶节段性肾小球硬化症(FSGS)大鼠模型,观察尿中脱落的肾小球足细胞的变化,并探讨其意义。方法FSGS组(n=7):采用左颈静脉插管一次性缓慢注射嘌呤霉素核苷酸(PAN,9mg/100g体重的方法建立)FSGS大鼠模型。正常对照组(n=5):注射等量生理盐水,实验周期20周。动态检测24h尿蛋白定量;间接免疫荧光方法动态检测尿沉渣足细胞特异性标志蛋白podocalyxin(PCX)、Wilm'stumor鄄1(WT鄄1);20周末肾组织光镜下观察肾小球病变;电镜观察肾小球足细胞的改变;免疫荧光染色观察肾小球内PCX和成熟足细胞特异性标志蛋白synaptopodin(PP44)的表达。结果FSGS组大鼠24h尿蛋白定量在第天较注射前明显升高,第312天达到高峰[(672.74±98.72)比(19.31±3.15)mg/24h,P<0.01),此后开始下降,于第6周接近注射前水平,持续至11周[(35.46±14.88)比(19.31±3.15)mg/24h,P=0.0238];从12周开始再度缓慢升高,持续高水平至20周,为注射前近7倍[(140.61±68.90)比(19.31±3.15)mg/24h,P<0.01]。FSGS组大鼠从12周开始,尿足细胞出现阳性(>1～5个/HP),持续至20周。光镜显示,30%～50%肾小球出现不同程度的局灶节段性硬化;电镜证实足突部分融合并可见足突与基底膜剥离。足细胞特异标记蛋白PCX、PP44在肾小球节段性硬化部位呈现节段性缺失。对照     

他克莫司对阿霉素肾病大鼠足细胞损伤的修复作用

目的探讨他克莫司对阿霉素肾病大鼠足细胞损伤的修复作用。方法通过阿霉素尾静脉注射建立大鼠微小病变肾病模型,并以他克莫司进行干预。大鼠随机分为对照组、模型组和他克莫司组。每组分别于第0、7、14、21、28、35天采集尿液,检测尿蛋白排泄量,于造模第35天处死大鼠收集肾脏标本。电镜观察各组大鼠足细胞足突融合情况;TUNEL检测法对肾小球进行染色;免疫组化或免疫荧光对WT-1、caspase-3进行定位和半定量检测,观察大鼠足细胞的数量和凋亡。结果阿霉素尾静脉注射后大鼠尿蛋白显著增加,足细胞数目明显减少,足突广泛融合;与模型组比较,他克莫司组大鼠24 h尿蛋白明显减少,足突融合改善,足细胞数目增多。与对照组比较,模型组大鼠肾小球内caspase-3蛋白表达增加,TUNEL染色加深;与模型组比较,他克莫司组肾小球内caspase-3表达量下降,TUNEL阳性率减少,说明足细胞凋亡减少。结论他克莫司可修复阿霉素肾病大鼠足细胞损伤,其机制与抑制足细胞凋亡有关。     

越婢汤对阿霉素肾病大鼠肾小球超微结构的影响

目的：观察越婢汤对阿霉素肾病（adriamycin nephropathy,AN）大鼠肾小球超微结构的影响。方法：尾静脉注射阿霉素6mg/kg建立AN大鼠模型,并随机分为空白组（A组）、模型组（B组）、越婢汤（C组）、激素（D组）、苯那普利（E组）,给予相应干预;第3周、7周留取肾皮质,以醋酸铀和柠檬酸铅双重染色法,H-600透射电镜观察GBM超微结构,并计数单位肾小球基底膜上足突个数。结果：（1）造模成功后与A组相比,模型组大鼠24h尿蛋白显著升高（P〈0.01）,血清Alb明显下降（P〈0.01）,血清TG和TC明显升高（P〈0.01）。（2）模型成功时透射电镜示模型组大鼠肾小球足突呈部分或弥漫性融合,单位长度基底膜上足突计数明显减少。（3）干预结束后与B组相比,C、D组超微结构明显改善,足突计数明显增加,且排列相对整齐（P〈0.01）。结论：越婢汤可改善AN大鼠肾小球超微结构,从而改善修复肾小球电荷屏障。     

南洋参对阿霉素肾病大鼠肾脏保护作用的初步研究

目的：观察南洋参对阿霉素肾病大鼠的肾脏保护作用.方法：18只雄性SD大鼠随机分为正常对照组（正常组,n=6）、阿霉素肾病组（模型组,n=6）和南洋参治疗组（治疗组,n=6）.模型组和治疗组大鼠一次性尾静脉注射阿霉素7.5 mg/kg诱导阿霉素肾病动物模型,正常组大鼠一次性尾静脉注射等量生理盐水.造模后第1天开始,治疗组大鼠每天以南洋参叶片水煎剂3 ml·500 g-1·d-1灌胃1次,正常组和模型组以蒸馏水3 ml·500 g-1·d-1灌胃,共治疗8周.留取各组大鼠1、4、8周尿标本并行24 h尿总蛋白定量检测,留取第8周时各组大鼠血清及肾脏组织标本,检测肾功能及血清蛋白等生化指标,并观察各组大鼠肾脏病理变化情况.结果：与正常组相比,模型组大鼠24 h尿蛋白定量从第1周开始已明显升高,第4、8周时治疗组较模型组有显著的降低.第8周时,模型组血清白蛋白（Alb）、总蛋白（TP）较正常组有显著降低,治疗组Alb较模型组明显升高,两组间血清总蛋白（TP）差异无统计学意义.模型组血清肌酐（Scr）、尿素氮（BUN）较正常组明显升高,治疗组较模型组明显降低.第8周时肾脏病理结果提示：模型组和治疗组较正常组均有明显肾小球硬化及肾小管间质的损伤,但治疗组的病变明显轻于模型组.结论：南洋参可以降低阿霉素肾病大鼠的蛋白尿水平,减轻肾脏病理损伤,延缓肾衰竭的进展,起到一定的肾脏保护作用.     

Adult and paediatric patients with minimal change nephrotic syndrome show no major alterations in glomerular expression of sulphated heparan sulphate domains.

BACKGROUND: Minimal change nephrotic syndrome (MCNS) is the most frequent form of nephrotic syndrome in childhood. In the glomerular basement membrane (GBM) of adult patients with MCNS, a reduced expression of a specific heparan sulphate (HS) domain has been reported. In children with MCNS, urinary activity of the HS-degrading enzyme heparanase was increased. It is, therefore, possible that a decreased GBM HS expression is associated with the pathogenesis of proteinuria in patients with MCNS. METHODS: In this study, HS in glomeruli of five adult and six paediatric patients with MCNS were analysed by immunofluorescence staining using four different antibodies, each defining a specific sulphated HS domain. The pediatric patients were subdivided into three groups depending on the presence or absence of podocyte foot process effacement, the level of proteinuria and prednisone administration at the time of the biopsy. In addition, kidneys of rats with adriamycin nephropathy (ADRN), a model for MCNS, were included in the study. RESULTS: Expression of sulphated HS domains was not aberrant in adult or paediatric patients compared with control subjects. Children with and without proteinuria had the same HS content. In contrast, rats with ADRN showed a decreased glomerular expression of sulphated HS domains. CONCLUSIONS: These results suggest that in patients with MCNS proteinuria is not associated with major changes in glomerular expression of sulphated HS domains.     

Podocyte foot process effacement as a diagnostic tool in focal segmental glomerulosclerosis

Podocyte foot process effacement is characteristic of proteinuric renal diseases. In minimal change nephrotic syndrome (MCNS) foot processes are diffusely effaced whereas the extent of effacement varies in focal segmental glomerulosclerosis (FSGS). Here we measured foot process effacement in FSGS and compared it to that in MCNS and in normal kidneys. A clinical diagnosis was used to differentiate idiopathic FSGS from secondary FSGS. Median foot process width, determined morphometrically by electron microscopy, was 3236 nm in 17 patients with idiopathic FSGS, 1098 nm in 7 patients with secondary FSGS, and 1725 nm in 15 patients with MCNS, as compared to 562 nm in 12 control patients. Multivariate analysis showed that foot process width did not correlate with proteinuria or serum albumin levels but was significantly associated as an independent factor with the type of disease. Foot process width over 1500 nm differentiated idiopathic from secondary FSGS with high sensitivity and specificity. Our results show that quantitative analysis of foot processes may offer a potential tool to distinguish idiopathic from secondary FSGS.     

Charge and size selectivity of proteinuria in children with idiopathic nephrotic syndrome

 Experimental studies have pointed to charge selectivity as an important determinant of glomerular permeability to macromolecules. Loss of glomerular basement membrane (GBM) polyanion has been proposed as a cause of the selective proteinuria in minimal change nephrotic syndrome (MCNS). However, the presence of less-anionic albumin in urine than plasma from MCNS and focal and segmental glomerulosclerosis (FSGS) patients has been interpreted both as evidence for partial maintenance of charge selectivity and for involvement of other pathogenic mechanisms. The exact role of charge selectivity in the pathogenesis of nephrotic proteinuria remains controversial. We have examined the clearance of endogenous proteins of differing size and charge in children with idiopathic nephrotic syndrome (NS). Chromatofocusing was used to determine the isoelectric points (pIs) of albumins in paired plasma and urine samples from patients with FSGS (n = 6) and MCNS (n = 6). Charge selectivity was assessed by comparing the pIs of the fractions with the highest albumin concentration (modal pI) in plasma and urine. The difference between the modal pIs was defined as the delta modal pI. Charge selectivity was also assessed from the albumin/transferrin and IgG4/IgG1 clearance ratios; size selectivity from the IgG1/albumin and IgG1/transferrin as well as the IgG4/albumin and IgG4/transferrin clearances. In children with FSGS, the mean (± SD) delta modal pI was  – 0.05 ± 0.16, and in MCNS  – 0.05 ± 0.11. Neither value differed significantly from zero. The albumin/transferrin clearance ratio showed no significant difference between FSGS and MCNS, but the IgG4/IgG1 clearance ratio was significantly higher in MCNS (P<0.05). Size selectivity was significantly reduced in FSGS compared with MCNS (for IgG1/transferrin P<0.01 and for IgG1/albumin P<0.05). For IgG4/transferrin and IgG4/albumin, P was <0.05. In conclusion, there was no evidence for residual charge selectivity in idiopathic NS associated with either MCNS or FSGS during nephrotic-range proteinuria. There was a significant loss of GBM size selectivity in children with FSGS with heavy proteinuria compared with children with MCNS with heavy proteinuria. Received August 7, 1996; received in revised form and accepted December 16, 1996     

Ultrastructural alteration of glomerular anionic sites in nephrotic patients

The relationship of glomerular anionic sites to proteinuria was examined ultrastructurally in human nephrotic syndrome. The anionic sites were analysed morphometrically in patients with minimal-change nephrotic syndrome (MCNS, 11 patients) and in other glomerulonephritides complicated with nephrotic syndrome (4 patients) by the high-iron diamine-thiocarbohydrazide-silver proteinate method. The anionic sites in MCNS patients in remission (7 patients) were normal. In contrast, the anionic sites in nephrotic patients with MCNS (4 patients) and the other glomerulonephritides were decreased in number. Moreover, smaller and irregularly distributed anionic sites or the greater loss of them from the paramesangial region were observed in the nephrotic patients. The loss of glomerular anionic sites may induce structural alteration of the glomerular basement membrane and mesangial matrix. The loss and structural abnormalities of glomerular anionic sites in nephrotic patients may be one of the mechanisms responsible for massive proteinuria.     

Podocyte foot process effacement is not correlated with the level of proteinuria in human glomerulopathies

BACKGROUND: Nephrotic syndromes result from increased glomerular permeability to proteins and are structurally believed to be associated with podocyte foot process effacement. Despite increasing knowledge of the molecular composition of the glomerular filtration barrier, the relationship between proteinuria and foot process effacement is unclear. METHODS: We conducted a morphologic study on the relationship between podocyte foot process effacement and proteinuria. Electron microscope pictures of glomerular capillaries were randomly taken from 27 cases in various stages of minimal change nephrotic syndrome (MCNS), from six cases of IgA nephropathy (IgAN) with high proteinuria and from seven control kidneys. From each picture, the mean width of the foot processes (FPW) was quantitated. RESULTS: In normal kidney the mean FPW was 580 +/- 40 nm. In biopsies from patients with MCNS without treatment, foot processes were diffusely effaced, reflected by a FPW of 1600 +/- 440 nm. In biopsies from patients with MCNS relapsing under prednisolone treatment, foot processes were significantly less effaced than in untreated MCNS (FPW 920 +/- 200 nm). In biopsies displaying IgAN, effacement was significantly more segmental than in untreated MCNS (FPW 800 +/- 170 nm). Proteinuria did not differ significantly among the groups. Neither in MCNS nor in IgAN was the extent of foot process effacement correlated with the level of proteinuria. CONCLUSION: Podocyte foot process effacement is not correlated with proteinuria. The differences in podocyte effacement between MCNS, MCNS relapsing under prednisolone treatment, and IgAN may point to different mechanisms of podocyte injury in these diseases.     

糖尿病大鼠肾脏α-辅肌动蛋白-4表达变化及作用机制

目的：动态观察肾小球足细胞骨架蛋白α-辅肌动蛋白-4（α-actinin-4）在糖尿病大鼠模型肾组织中表达的变化,探讨α-actinin-4与蛋白尿发生的关系及导致其出现变化的可能机制。方法：将SD大鼠随机分为两组：对照组及糖尿病组,腹腔注射链脲佐菌素（STZ）制作糖尿病大鼠模型,分别于2、4、6、8周末检测每组大鼠24h尿蛋白定量并处死大鼠留取肾标本。电镜观察足细胞超微结构的变化;应用酶免法检测肾组织糖基化终产物（AGEs）的含量;应用免疫组化及Western-blot检测α-actinin-4蛋白的表达;RT-PCR检测α-actinin-4mRNA表达量的变化。结果：6周糖尿病组大鼠24h尿蛋白明显高于对照组（P〈0.01）,增高持续到8周（P〈0.01）;透射电镜显示8周糖尿病组大鼠足突出现节段性融合;从4周时糖尿病组大鼠肾组织AGEs含量明显升高（P〈0.05）,并持续到8周（P〈0.01）;与对照组相比,从4周时糖尿病组大鼠肾组织α-actinin-4蛋白表达明显降低（P〈0.05）,并持续到8周（P〈0.05）;与对照组相比,从2周时糖尿病组大鼠肾组织α-actinin-4mRNA表达明显降低（P〈0.05）,并持续到8周（P〈0.01）。结论：α-actinin-4表达降低参与了糖尿病大鼠蛋白尿的发生,而AGEs可能是导致α-actinin-4表达下调的原因之一。     

不同病理类型肾综患者尿蛋白对肾小管上皮细胞增殖和凋亡相关蛋白Fas表达的影响

目的：观察不同病理类型肾病综合征（NS）患者尿蛋白对肾小管上皮细胞（RTECs）增殖和凋亡的影响,以进一步明确尿蛋白所致肾小管-间质损害的机制.方法：（1）从局灶-节段性肾小球硬化症（FSGS）、膜性肾病（MN）、微小病变肾病（MCN）三种不同病理类型的NS患者尿液中提取尿蛋白,经成份分析、灭菌等处理后以0.5 mg/ml、1.0 mg/ml、2 mg/ml、4 mg/ml、8 mg/ml浓度分别刺激体外培养的HK-2细胞,另设空白对照组.（2）MTT法检测不同病理类型NS患者尿蛋白刺激后细胞的增殖情况.（3）乳酸脱氢酶（LDH）释放实验检测不同病理类型NS患者尿蛋白的细胞毒作用.（4）Western Blotting法检测Fas蛋白表达.结果：各病理类型所提取的尿蛋白成分相同,主要为白蛋白、转铁蛋白、IgG等,但各病理类型组成比例不同;肾小管上皮细胞MTT值低浓度有明显增殖作用,高浓度时细胞过度增殖则导致凋亡;肾小管上皮细胞LDH释放率和Fas蛋白的表达水平随尿蛋白浓度的升高而升高;以上各项检测指标中FSGS患者尿蛋白对HK-2细胞的作用最强,MN次之,MCD最弱.结论：在体外条件下,尿蛋白对RTECs呈剂量依赖性的细胞毒作用,低剂量尿蛋白诱导RTECs异常增殖,较高剂量尿蛋白可诱导RTECs凋亡;除尿蛋白的量决定了损伤严重程度外,尿蛋白的性质也决定了损伤的严重程度.     

Expression of complement regulatory proteins on erythrocytes from patients with idiopathic focal segmental glomerulosclerosis

SUMMARY: Focal segmental glomerulosclerosis (FSGS) is a heterogeneous group of disorders with respect to aetiology, morphology, clinical course and response to treatment. The present study assessed the expression of complement receptor 1 (CR1), decay accelerating factor (DAF) and membrane inhibitor of reactive lysis (CD59) on the erythrocytes of FSGS patients using flow cytometry compared with their expression on the erythrocytes of minimal change nephrotic syndrome (MCNS) patients. Significantly reduced expression of CR1, DAF and CD59 was observed on the erythrocytes of FSGS patients compared with the reduced expression of CR1 and enhanced expression of DAF on the erythrocytes of MCNS patients. A significant inverse relationship was demonstrated between CR1 expression and proteinuria levels in FSGS patients ( r = 0.55, P < 0.01). A follow-up study of 12 patients with FSGS after immunosuppressive therapy showed that the levels of complement regulatory proteins are significantly increased when the disease goes into remission. However, in patients not responding to immunosuppressive therapy, levels of these proteins remained low. MCNS patients showed significant increases in CR1 and decreases in DAF expression during remission of the disease.