本文選題：幽門(mén)螺桿菌感染　切入點(diǎn)：IgA腎病　出處：《四川醫(yī)科大學(xué)》2015年碩士論文　論文類(lèi)型：學(xué)位論文

【摘要】：目的:Ig A腎病是全球范圍內(nèi)最常見(jiàn)的原發(fā)性腎小球疾病,在我國(guó)已成為導(dǎo)致慢性腎功能衰竭最主要的腎小球疾病,大約30%~50%的患者在疾病診斷后20年內(nèi)發(fā)展到終末期腎衰竭(ESRD);目前,幽門(mén)螺桿菌(Hp)感染備受關(guān)注,已有研究提示Hp感染可能與Ig A腎病發(fā)病有關(guān)。我們前期體外研究證實(shí)幽門(mén)螺旋桿菌感染或毒力因子Cag A可通過(guò)刺激B淋巴細(xì)胞增殖、影響Ig A1分泌以及低糖基化參與Ig A腎病的發(fā)生,但是尚缺乏臨床證據(jù)。本研究擬通過(guò)檢測(cè)Ig A腎病患者Hp感染情況,研究分析Hp感染與Ig AN臨床預(yù)后之間的關(guān)系,并檢測(cè)Hp感染對(duì)Ig A腎病患者Ig A1的產(chǎn)生、Ig A1糖基化的影響以及腎組織中Hp抗原和Cag A的沉積情況,尋找Hp參與Ig A腎病的臨床證據(jù)。方法:收集經(jīng)腎病理活檢確診為原發(fā)性腎小球疾病患者42例,排除繼發(fā)性腎病,包括Ig A腎病患者22例和非Ig AN的原發(fā)性腎小球疾病患者20例,采用14C-尿素呼氣試驗(yàn)、酶聯(lián)免疫吸附法(ELISA)檢測(cè)Hp感染情況,酶聯(lián)免疫吸附法(ELISA)法檢測(cè)血清中Ig A1濃度,HAA凝集素結(jié)合試驗(yàn)法檢測(cè)Ig A1低糖基化程度,運(yùn)用免疫組織化學(xué)方法檢測(cè)腎組織中Hp抗原及Cag A沉積情況,同時(shí)收集患者臨床資料、血Ig A、補(bǔ)體C3、血肌酐、24h尿蛋白定量、估算腎小球?yàn)V過(guò)率、病理指標(biāo)結(jié)果。結(jié)果:1、14C-尿素呼氣實(shí)驗(yàn)結(jié)果顯示,Ig AN患者Hp現(xiàn)癥感染率與n-Ig AN患者及健康人無(wú)明顯差異;但ELISA結(jié)果顯示Ig AN患者血清Hp-Ig G抗體的陽(yáng)性率顯著高于n-Ig AN患者及健康人(P0.05)。2、Ig AN患者中,Hp陽(yáng)性患者血清Ig A1分子濃度及其與HAA凝集素的結(jié)合能力均高于Hp陰性患者。3、Ig AN患者中,Hp感染陽(yáng)性患者與Hp感染陰性患者相比,血Ig A及Ig A/C3比值增高,24h尿蛋白低及估算腎小球?yàn)V過(guò)率降低。4、Hp抗原及Cag A均在腎小管沉積,且沉積部位一致,而在腎小球部位無(wú)陽(yáng)性發(fā)現(xiàn)。Ig AN患者腎組織Hp抗原及Cag A沉積程度顯著高于n-Ig AN患者。Ig AN患者中,Hp感染陽(yáng)性患者腎組織中Hp及Cag A沉積陽(yáng)性率顯著高于Hp感染陰性患者。而n-Ig AN患者中,Hp感染陽(yáng)性患者與Hp感染陰性患者無(wú)差異。結(jié)論:Ig AN患者與n-Ig AN患者及健康人Hp現(xiàn)癥感染率相似。幽門(mén)螺旋桿菌通過(guò)誘導(dǎo)強(qiáng)烈免疫反應(yīng),使Ig AN患者體內(nèi)針對(duì)Hp感染的抗體顯著增加,促進(jìn)機(jī)體Ig A1分泌以及低糖基化,并加重腎功能損害。Hp抗原及Cag A均在腎組織的腎小管部位沉積,且Ig AN患者腎組織Hp抗原及Cag A沉積程度顯著增高;Hp感染可顯著增加Ig AN患者腎組織中Hp抗原及Cag A沉積機(jī)會(huì)。研究提示幽門(mén)螺旋桿菌感染可能在Ig A腎病的發(fā)病機(jī)制中起到直接的病理作用,其機(jī)制可能與介導(dǎo)腎小管損傷相關(guān),清除幽門(mén)螺桿菌可能有助于幽門(mén)螺桿菌感染陽(yáng)性的Ig A腎病患者的治療。
[Abstract]:Objective: IgA nephropathy is the most common primary glomerular disease in the world, and it has become the most important glomerular disease leading to chronic renal failure in China. About 30 percent of patients develop end stage renal failure within 20 years of diagnosis; currently, Helicobacter pylori (HP) infection is a major concern. Previous studies have shown that HP infection may be related to the pathogenesis of IgA nephropathy. Our previous studies in vitro have demonstrated that Helicobacter pylori infection or virulence factor Cag A can stimulate B lymphocyte proliferation. The effect of Ig A1 secretion and low glycosylation on the pathogenesis of IgA nephropathy, but there is still no clinical evidence. This study is to study the relationship between HP infection and clinical prognosis of IgA nephropathy patients by detecting HP infection in patients with IgA nephropathy, and analyzing the relationship between HP infection and clinical prognosis of IgA nephropathy. The effect of HP infection on the production of IgA1 in patients with IgA nephropathy and the deposition of HP antigen and Cag A in renal tissue were detected. Methods: 42 cases of primary glomerular disease diagnosed by biopsy of nephropathy were collected to exclude secondary nephropathy. 22 patients with IgA nephropathy and 20 patients with non-IgAN primary glomerular disease were tested for HP infection by 14C- urea breath test and Elisa. Enzyme linked immunosorbent assay (Elisa) was used to detect the concentration of IgA1 in serum and the level of low glycosylation of IgA1 was detected by HAA agglutinin binding assay. HP antigen and Cag A deposition in renal tissue were detected by immunohistochemical method. The clinical data of the patients were collected at the same time. Serum IgA, complement C3, serum creatinine, 24 hours urinary protein, glomerular filtration rate and pathological index were estimated. Results the HP infection rate of patients with Ig an was not significantly different from that of n-Ig an patients and healthy persons. The results of ELISA showed that the positive rate of serum Hp-Ig G antibody in patients with IgAN was significantly higher than that in patients with n-Ig an and healthy controls. The concentration of IgA1 and its binding ability with HAA agglutinin in patients with HP positive were higher than those in patients with HP negative. (3) HP infection positive patients in Ig an patients were compared with those with HP negative infection. The increase of serum IgA and IgA / C3 ratio and the decrease of 24 hours urinary protein and the decrease of estimated glomerular filtration rate. 4 HP antigen and Cag A were deposited in renal tubules, and the deposition site was the same. However, there was no positive rate of HP and Cag A deposition in renal tissue in patients with IgAN and n-IgAN patients. The positive rates of HP and Cag A in renal tissues of patients with Hp-positive infection were significantly higher than those of patients with HP infection in n-IgAN patients. There was no difference between the patients with positive HP infection and those with negative HP infection in n-Ig an patients. Conclusion the infection rate of HP in patients with 1% Ig an is similar to that in patients with n-Ig an and healthy people. Helicobacter pylori induces strong immune response. The antibody against HP infection was significantly increased in IgAN patients, which promoted the secretion of IgA1 and low glycosylation, and aggravated the renal function damage. HP antigen and Cag A were deposited in the renal tubules of renal tissue. HP antigen and Cag A deposition in renal tissue of patients with IgAN increased significantly. HP infection in renal tissue of IgAN patients increased the chances of HP antigen and Cag A deposition in renal tissue of IgAN patients. It is suggested that Helicobacter pylori infection may occur in IgA nephropathy. Play a direct pathological role in the pathogenesis of the disease, The mechanism may be related to mediated renal tubular injury and the clearance of Helicobacter pylori may contribute to the treatment of patients with HP positive IgA nephropathy.
【學(xué)位授予單位】：四川醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類(lèi)號(hào)】：R692.31

【參考文獻(xiàn)】

相關(guān)期刊論文 前1條

1 張萬(wàn)岱;胡伏蓮;蕭樹(shù)東;徐智民;;中國(guó)自然人群幽門(mén)螺桿菌感染的流行病學(xué)調(diào)查[J];現(xiàn)代消化及介入診療;2010年05期

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本文編號(hào)：1618624