本文選題：終末期腎病 + 脂聯(lián)素　； 參考：《右江民族醫(yī)學(xué)院》2017年碩士論文

【摘要】：目的:探討脂聯(lián)素(Adiponectin,ADPN)及相關(guān)炎癥因子在終末期腎病(End-Stage Renal Disease,ESRD)并頸動脈粥樣硬化(Carotid atherosclerosis,CAS)患者體內(nèi)的表達(dá)及相關(guān)性,并分析其在CAS形成中的可能分子機制。方法:采用病例-對照研究,選取2015年3月至2016年3月在我院腎內(nèi)科住院治療并確診為頸動脈粥樣硬化的ESRD患者64例為實驗組(即ESRD組),頸動脈粥樣硬化的非慢性腎臟病(Chronic Kidney Disease,CKD)患者42例為陽性對照組(即非CKD組),同期健康體檢者30例為正常對照組。采用酶聯(lián)免疫吸附法檢測外周血清脂聯(lián)素、腫瘤壞死因子-ɑ(Tumor Necrosis Factor Alpha,TNF-α)的濃度;肌氨酸氧化酶法檢測血清肌酐;脲酶連續(xù)監(jiān)測法檢測血清尿素氮;免疫透射比濁法檢測血清C反應(yīng)蛋白(C Reactive Protein,CRP);采用實時熒光定量PCR(Real-Time PCR,RT-PCR)法檢測外周血單個核細(xì)胞脂聯(lián)素DNA表達(dá)水平;采用高分辨超聲技術(shù)檢測頸動脈內(nèi)膜-中層厚度(Internal Carotid Artery IntimaMiddle Thickness,IMT)及粥樣硬化斑塊。所有數(shù)據(jù)采用均數(shù)±標(biāo)準(zhǔn)差表示,各組間比較采用單因素方差分析,相關(guān)性分析采用pearson相關(guān)分析,獨立危險因素分析采用多因素Logistic回歸分析。結(jié)果:ESRD組的CRP、TNF-ɑ、IMT分別為11.18±8.62 mmol/L、37.69±12.73ng/L和0.79±0.13 mm,高于正常對照組的4.28±3.86 mmol/L、30.30±9.96 ng/L和0.56±0.10 mm(均P0.01),低于非CKD組的18.19±11.67 mmol/L、124.86±37.86ng/L和0.98±0.14mm(均P0.01);ADPN為46.20±10.62μg/mL,高于正常對照組(13.15±4.33μg/mL)和非CKD組(4.99±1.48μg/mL)(均P0.01);ADPN mRNA相對表達(dá)量為0.185±0.121,低于正常對照組(1.502±1.09)(P0.01),與非CKD組(0.184±0.095)比較差異無統(tǒng)計學(xué)意義;ADPN與BUN、Scr、eGFR的相關(guān)系數(shù)分別為0.634、0.638、-0.871(均P0.01);ADPN與CRP、TNF-ɑ、IMT的相關(guān)系數(shù)分別為-0.307、-0.779和-0.538(均P0.01);CRP與BUN、Scr、eGFR的相關(guān)系數(shù)分別為0.952、0.832、-0.925(均P0.01);TNF-ɑ與BUN、Scr、eGFR的相關(guān)系數(shù)分別為0.973、0.862、-0.916(均P0.01);IMT與CRP、TNF-ɑ的相關(guān)系數(shù)分別為0.912和0.896(均P0.01);CRP、TNF-ɑ的OR值分別為27.376和36.512,95%CI值分別為1.935~387.325和1.335~998.385。結(jié)論:(1)ESRD并發(fā)CAS患者存在ADPN mRNA低表達(dá)和血清ADPN濃度升高現(xiàn)象,ADPN與eCFR呈負(fù)相關(guān),提示ADPN血清濃度升高可能不是mRNA調(diào)控所致,而受腎功能影響;(2)ESRD并發(fā)CAS患者存在微炎癥狀態(tài),IMT與CRP、TNF-α呈正相關(guān),CRP、TNF-α是ESRD患者并發(fā)CAS的獨立危險因素;(3)ESRD并發(fā)CAS患者ADPN與IMT、CRP、TNF-α呈負(fù)相關(guān),ADPN可能具有抑制炎癥反應(yīng)及抑制ESRD患者動脈粥樣硬化的作用。
[Abstract]:Objective: to investigate the expression and correlation of adiponectin Adiponectin (ADPN) and related inflammatory factors in patients with end-stage nephropathy (ESRD) and carotid atherosclerosis (CAS), and to analyze its possible molecular mechanism in the formation of CAS. Methods: a case-control study was conducted. From March 2015 to March 2016, we selected 64 ESRD patients who were hospitalized in our hospital from March 2015 to March 2016 and diagnosed carotid atherosclerosis as experimental group (ESRD group). 42 patients with carotid atherosclerosis were treated with Chronic Kidney Disease CKD. Sex control group (non-CKD group), 30 cases of health check-up at the same time as the normal control group. Serum levels of adiponectin, Tumor Necrosis Factor Alpha-TNF- 偽, creatinine oxidase and urea nitrogen in serum were detected by enzyme-linked immunosorbent assay (Elisa). Serum C-reactive protein was detected by immunoturbidimetry and adiponectin DNA expression in peripheral blood mononuclear cells (PBMC) was detected by real-time fluorescence quantitative PCR- Real-Time PCR- (RT-PCRR) method, and immunoturbidimetric assay was used to detect the expression of adiponectin DNA in peripheral blood mononuclear cells (PBMC). Carotid intima-media thickness (IMT) and atherosclerotic plaque were detected by high resolution ultrasound. All the data were expressed as mean 鹵standard deviation. The analysis of variance of single factor, pearson correlation analysis and multivariate logistic regression analysis were used in correlation analysis and independent risk factor analysis. 緇撴灉:ESRD緇勭殑CRP,TNF-蓱,IMT鍒嗗埆涓，

本文編號：2044272