Nycocard金标法定量检测晨尿微量白蛋白的临床应用

尿微量白蛋白（？db）已被公认为糖尿病肾病的早期诊断指标，但尿液收集及测定尿微量Alb的方法各不相同，24h尿放射免疫测定（RIA）法检测尿微量Alb是公认的方法，我们以此为金标准观察Nycocard金标法检测晨尿微量Alb的可靠性，为临床提供一种简单且精确的测定方法。     

IgA肾病患者血清IgA1与系膜细胞共培养上清诱导足细胞凋亡

目的 探讨IgA肾病(IgAN)患者血清IgA1与系膜细胞共培养上清对足细胞凋亡的影响。 方法 用Jacalin 亲和层析柱和Sephacryl S-200 分子筛纯化蛋白。单体IgA1（mIgA1）热聚合为聚合体IgA1（aIgA1）。实验分为患者上清组、健康上清组和对照组，系膜细胞分别与IgAN患者的aIgA1、健康对照的aIgA1和5%胎牛血清共培养，收集上清，与同步化的足细胞作用。流式细胞仪检测细胞凋亡情况。实时定量PCR 检测凋亡相关基因Bcl-2、Bax、Fas和Fas-L表达情况。 结果 患者上清可诱导足细胞凋亡，其凋亡率显著高于健康上清组和对照组[（28.5±5.9）%比（22.5±5.8）%、（20.5±4.5）%， 均P < 0.05]。患者上清可诱导足细胞Fas mRNA 升高，为对照组的1.89倍（P < 0.05）， 而Bcl-2 mRNA下调为对照组的72%（P < 0.05）。患者上清组的AngⅡ和TGF-β1水平均高于健康上清组[（13.2±3.4） ng/L比（8.2±2.3） ng/L，P < 0.05；（15.4±3.4） ng/L比（10.8±3.2） ng/L，P < 0.05]。 结论 IgAN患者血清IgA1与系膜细胞共培养上清可诱导足细胞凋亡，可能参与IgAN的进展。     

Urinary podocytes in childhood IgA nephropathy

SUMMARY: We have previously demonstrated the presence of detached podocytes in the urine in various glomerular diseases. In this study, we investigated the pathological significance of detachment of urinary podocytes (u-podocytes) in childhood IgA nephropathy. We investigated 28 children with IgA nephropathy. U-podocytes were detected in the urinary sediment by immunofluorescence. Renal pathological changes and urinalysis, including the u-podocyte test, were analysed. The expression of glomerular basement membrane (GBM) components, integrins and cytoskeleton components on urinary podocytes was investigated using dual immunofluorescence in 12 patients. The u-podocyte score paralleled the acute glomerular changes in renal biopsy samples. The infiltration of glomerular macrophages and polymorphonuclear leucocytes, and the number of urinary leucocytes, correlated highly with the u-podocyte score. Some of the u-podocytes expressed integrins and also components of the GBM. Detachment of podocytes reflects the presence of acute glomerular lesions. Infiltration of glomerular leucocytes is considered to be the cause of the detachment, partly because of the destruction of the GBM.     

Development and testing of an artificial intelligence tool for predicting end-stage kidney disease in patients with immunoglobulin A nephropathy

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痹祺胶囊联合甲氨蝶呤治疗类风湿关节炎的临床研究

目的 观察痹祺胶囊联合甲氨蝶呤治疗类风湿关节炎的临床疗效。方法 选取2018年5月—2020年12月邯郸市中心医院收治的200例类风湿关节炎患者，根据信封抽签法将患者分为对照组和观察组，每组各100例。对照组温水送服甲氨蝶呤片，7.5 mg/次，1次/周。观察组在对照组的基础上温水送服痹祺胶囊，4粒/次，3次/d。两组连续治疗12周。观察两组患者的临床疗效，同时比较两组C反应蛋白（CRP）、类风湿因子滴度（RF）、抗链球菌溶血素"O"（ASO）、红细胞沉降率（ESR）、免疫球蛋白A（IgA）、免疫球蛋白G（IgG）、免疫球蛋白M（IgM）及补体C3、C4水平。结果 治疗后，观察组的临床总有效率为83.00%，显著高于对照组的69.00%（P<0.05）。治疗后，两组CRP、ASO、ESR和RF水平均显著下降（P<0.05）；治疗后，观察组的风湿四项指标水平显著低于对照组（P<0.05）。治疗后，两组IgG、IgA、IgM均较治疗前下降（P<0.05）；治疗后，观察组的IgA、IgM、IgG均低于对照组（P<0.05）。两组治疗前后补体C3、C4组间对比均未见统计学差异。结论 痹祺胶囊联合甲氨蝶呤治疗类风湿关节炎患者，可有效控制疾病进展，调节血清免疫球蛋白水平，提高治疗效果。     

IgA肾病肾病综合征临床病理特点及肾脏病理危险因素

目的：探讨IgA肾病肾病综合征患者临床病理特点及肾脏病理损害的危险因素。方法：选择1987年～2006年经肾活检确诊IgA肾病并表现为肾病综合征的患者118例，分析其临床病理特点，按肾脏病变轻重分为A组（n=34，包括Lee氏分级Ⅰ级、Ⅱ级）、B组（n=84，Ⅲ、Ⅳ、Ⅴ级），比较两组临床指标，并多因素分析影响肾脏病理损害的危险因素。结果：A、B两组高血压分别占11．8％ vs 63．1％；肾衰竭分别占15％ vs 41．7％；A、B两组尿蛋白≥6g／24h者分别占58．8％ vs 32．1％；尿红细胞满视野分别为14．7％ vs 50％。A组高血压、肾衰竭、镜下尿红细胞满视野发生率显著低于B组（P〈0．01），尿蛋白≥6g／24h发生率显著高于B组（P〈0．01）。A组平均动脉压、血肌酐明显低于B组（P〈0．01）；而尿蛋白定量、血红蛋白显著高于B组（P〈0．05）。多因素分析显示IgA肾病肾病综合征患者肾脏病理损害重的危险因素有平均动脉压、尿蛋白〈6g／24h、镜下尿RBC〉5．0×10^7／L（0R值分别为1．048，3．227，6．578；P值分别为0．034，0．047，0．002），血红蛋白是保护性因素（OR=0.723，P=0．035）。随着平均动脉压的升高、血红蛋白的降低、镜下尿红细胞数的增多，肾脏病理损害程度加重（P〈0．01）。结论：IgA肾病肾病综合征患者临床、病理表现存在差异，高血压、血红蛋白水平、24h尿蛋白排泄量、镜下尿红细胞程度有助于判断肾脏病理损害轻重。     

尿激酶对IgA肾病毛细血管密度的影响

目的:观察尿激酶治疗后IgA肾病毛细血管密度的变化.方法:观察不同病理程度下,IgA肾病毛细血管密度的变化,同时比较尿激酶治疗前后,10例重复肾活检IgA肾病患者的毛细血管密度变化.结果:①随着病变的加重,IgA肾病肾小球毛细血管袢密度、肾小管周围毛细血管密度均随之减小.② 10例IgA肾病应用尿激酶治疗后,重复肾活检显示,治疗前后肾小球毛细血管袢密度(/肾小球)分别为:36.5±8.7和45.4±9.9,两者相比具有统计学差异(P<0.05),肾小管周围毛细血管密度(/肾小管)明显升高(治疗前0.9±0.2 vs治疗后1.4±0.3,P<0.05).结论:尿激酶治疗可能是通过增加肾小球和肾间质毛细血管的密度而延缓IgA肾病的进展.     

A case of nephrotic syndrome 11 yr post-kidney transplantation

Abstract:  We present here a male patient who had developed nephrotic syndrome 11 yr after kidney transplantation. Nephrotic syndrome suddenly occurred after severe sunburn he got in Hawaii. Such a clinical course seemed very rare in kidney transplantation, and multifactorial etiology was suspected. The histological findings of graft biopsy were intricate. On light microscopy, there were mesangial expansion and endocapillary proliferation with duplication of GBM and crescent formation. Deposits of IgM in mesangium were the most prominent finding on immunofluorescence microscopy, but IgA and C3 deposits were also detected. Electron microscopy revealed paramesangial and a few subepithelial dense deposits. Additionally, small organized deposits were found in the subepithelial space. Based on these findings, a provisional diagnosis of IgA nephropathy superimposed on chronic transplant glomerulopathy was made. However, hepatitis C virus related nephropathy could not be excluded.     

Urinary transforming growth factor-β1 is an indicator of histological chronicity in IgA nephropathy

SUMMARY: This study examined urinary excretion of transforming growth factor-β1 (TGF-β1) in adult IgA nephropathy and compared this with clinical and histological parameters. TGF-β1 was measured by enzyme-linked immunosorbent assay in 24-h urine specimens from 25 patients with IgA nephropathy (17 men, eight women). Urine from eight age-matched control subjects served as the control. Serum TGF-β1 was also measured in 16 out of the 25 patients and six age-matched control subjects. TGF-β1 was detected in the urine in 72% of IgA nephropathy patients(18/25), but was not detected in any of the control subjects. Patients with decreased renal function (creatinine clearance (Ccr) < 80 mL/min) had higher urine levels of TGF-β1 than those with normal renal function (Ccr ≥ 80 mL/min) (141.8 ± 60.0 ng/day vs 39.7 ± 33.2 ng/day, P < 0.01). The level of TGF-β1 gave a negative correlation with Ccr ( r = −0.62, P = 0.001), but not with proteinuria ( r = 0.11, P = 0.58). Twenty-two of the patients were evaluated histologically. The urinary TGF-β1 levels correlated with both global sclerosis and interstitial volume ( r = 0.52, P < 0.05, and r = 0.51, P < 0.05, respectively). However, there was no correlation between TGF-β1 levels and glomerular intracapillary inflammatory cell score, mesangial proliferation score or the matrix score. No correlation was found between TGF-β1 levels and the number of glomerular or interstitial CD68⁺ cells. No significant differences in serum TGF-β1 levels were observed between patients with normal Ccr and those with decreased Ccr. Also, its levels were found to be independent of the urine levels. In conclusion, 24-h urinary TGF-β1 excretion was found to correlate with Ccr, global sclerosis and interstitial volume, demonstrating that urinary TGF-β1 is an indicator of chronicity in adult IgA nephropathy.