Apelin在肾血管性高血压大鼠模型中的浓度及意义

目的观察Apelin在肾血管性高血压大鼠模型中的含量以及与血管紧张素Ⅱ(AngⅡ)、一氧化氮(NO)的相关性,探讨Apelin在肾血管性高血压中的作用。方法将20只雄性180～220gWistar大鼠随机分为手术组和假手术组。在术后4周测量平均颈动脉压,确定模型制备成功。ELISA法测定血浆Apelin-12、AngⅡ、NO浓度,分析其相关性;免疫组化法检测心脏Apelin-12蛋白表达。分析手术组与假手术组平均颈动脉压、血浆Apelin-12、AngⅡ、NO浓度变化和心脏组织Apelin-12表达情况。结果平均颈动脉压手术组与假手术组相比显著增高(P<0.01)。血浆中Apelin-12及AngⅡ浓度手术组高于假手术组(P<0.01);血浆中NO浓度手术组低于假手术组(P<0.01)。心脏组织中Apelin-12蛋白表达手术组高于假手术组。手术组血浆中Apelin-12浓度与AngⅡ浓度呈正相关(r=0.877,P<0.01),与NO浓度呈负相关(r=-0.853,P<0.01)。结论 Apelin-12可能在肾血管性高血压的病理生理发展过程中发挥作用。Apelin-12、AngⅡ、NO共同参与肾血管性高血压的发生发展过程,Apelin-12可能通过AngⅡ、NO发挥作用。     

Apelin-13对高血压性肾纤维化的影响及机制研究

目的探讨血管紧张素受体AT1相关的受体蛋白(APJ)激动剂Apelin-13对高血压性肾纤维化的影响及其机制。方法 12周龄雄性自发性高血压大鼠随机分为对照组、1μg/(kg·d)Apelin-13组、10μg/(kg·d)Apelin-13组、100μg/(kg·d)Apelin-13组;Apelin-13通过尾静脉给药。测量大鼠24 h尿蛋白量、血清肌酐和尿素氮浓度。采用套尾法测量尾动脉收缩压,HE染色和Masson染色观察大鼠肾脏组织学改变,Western blot检测肾脏组织中自噬相关蛋白微管相关蛋白1轻链3(LC3)、Beclin-1和p62的表达。结果与对照组比较,10μg/(kg·d)Apelin-13组、100μg/(kg·d)Apelin-13组以剂量依赖方式降低大鼠收缩压、24 h尿蛋白量、血清肌酐和尿素氮水平、肾脏损伤评分和胶原容积分数(均P0.05),减轻肾小管上皮细胞水肿,减少间质胶原沉积,降低肾间质纤维化程度。10μg/(kg·d)Apelin-13组、100μg/(kg·d)Apelin-13组也以剂量依赖方式增加大鼠肾脏组织中LC3-Ⅱ表达和LC3-Ⅱ/LC3-Ⅰ比值及Beclin-1表达,降低p62表达(均P0.05)。结论 Apelin-13抑制高血压性肾纤维化的进展,其机制可能与Apelin-13抑制细胞自噬有关。     

老年IgA肾病患者的临床病理特点和长期预后的相关危险因素分析

目的:探讨老年IgA肾病(IgAN)患者的临床病理特点、长期预后及其相关危险因素. 方法:选取2003年1月至2012年12月在南京军区南京总医院肾脏科经肾活检确诊为IgAN且年龄≥65岁的患者82例,随机选取同期经肾活检确诊为IgAN且年龄在18～64岁的患者328例作为对照组,回顾性分析这些患者的临床及随访资料. 结果:老年IgAN患者与对照组相比,肾活检时平均动脉压(MAP) (P=0.001)、24h尿蛋白定量(P=0.011)、血清肌酐(P＜0.001)、估算的肾小球滤过率(eGFR)(P＜0.001)、血尿酸(P=0.012)、总胆固醇水平(P＜0.001)均存在统计学差异.老年IgAN肾小球硬化比例(P=0.001)及肾小管萎缩/间质纤维化(P=0.009)、肾小球节段硬化(P＜0.001)和动脉硬化(P＜0.001)等慢性化病变的发生率均明显高于对照组.老年IgAN患者3年和8年累计肾脏存活率分别为(89.6％和37.7％,P=0.000 2),显著低于对照组(96.5％和79.4％,P=0.000 2).多因素COX回归分析结果表明,肾活检时蛋白尿(HR 1.847;P=0.011)、eGFR(HR 1.080;P=0.006)水平及存在肾小管萎缩/间质纤维化(HR 5.850; P=0.007)是老年IgAN患者肾脏预后的独立危险因素. 结论:本研究表明,老年IgAN患者高血压、血清肌酐升高及肾病范围蛋白尿的发生率均高于同期行肾活检的非老年IgAN患者,肾脏组织的慢性化病变突出.肾活检时蛋白尿、eGFR水平及存在肾小管萎缩/间质纤维化是影响老年IgAN患者预后的独立危险因素.     

特发性膜性肾病30例肾小管上皮细胞自噬改变及其临床意义

目的观察特发性膜性肾病(idiopathic membranous nephropathy,IMN)患者肾小管自噬体数量、自噬相关蛋白Beclin-1和LC3的表达,了解肾小管上皮细胞自噬是否参与了IMN肾间质纤维化的进展。方法回顾性总结2015年6月至2016年12月在中国医科大学附属盛京医院经肾活检确诊为IMN患者30例,在透射电子显微镜下观察IMN患者肾组织肾小管上皮细胞自噬体的数量,免疫组化检测自噬相关蛋白Beclin-1和LC3的表达,分析其与24 h尿蛋白定量、肾间质纤维化程度及肾功能等临床相关指标的相关性。结果与正常肾组织相比,IMN组的肾小管上皮细胞自噬体数量、自噬相关蛋白Beclin-1和LC3表达显著增加(t=-13.266,P0.001;t=-5.261,P0.001;t=-2.394,P=0.026);在IMN组中,与无纤维化组相比,有纤维化组自噬小体数量、Beclin1和LC3表达均显著增加(t=-6.04,P0.001;t=-2.795,P=0.014;t=-2.761,P=0.004);在IMN患者中,自噬小体数量、Beclin1和LC3均与患者肾间质纤维化累及面积成正相关(r分别为0.757、0.658和0.638,均P0.001);LC3与24 h尿蛋白定量成负相关(r=-0.463,P=0.01),Beclin1与血清尿素氮(BUN)成正相关(r=0.433,P=0.017),自噬小体数量与患者性别具有一定的相关性(r=-0.472,P=0.008)。结论在IMN患者中,肾小管上皮细胞自噬参与了肾间质纤维化的进展。     

狼疮肾炎患者肾组织中结缔组织生长因子的转录表达及意义

目的探讨人类狼疮肾炎(LN)患者肾组织中结缔组织生长因子(CTGF)的基因转录和蛋白表达与肾纤维化之间的关系。方法应用免疫组织化学和原位杂交技术,以15例正常肾组织为对照,观察了36例LN患者肾组织中CTGF表达的分布和表达量的变化,分析肾组织中CTGF表达与LN肾间质病变的内在联系。结果LN患者肾组织的CTGF表达主要分布在肾小管上皮细胞和肾间质细胞、肾小球脏层和壁层上皮细胞和系膜区细胞。正常肾组织没有或只有极弱的CTGFmRNA转录和蛋白表达;LN患者肾组织CTGFmRNA转录及蛋白表达量较正常肾组织显著增高(CTGFmRNA:8.22±3.13比1.12±0.23;CTGF蛋白:8.74±3.24比1.21±0.22,P均<0.001);LN患者肾组织CTGF表达量与肾间质病变程度呈正相关(r=0.863,P<0.01);Ⅳ型LN患者肾组织CTGF表达量显著高于非Ⅳ型LN患者(CTGFmRNA:10.73±3.61比4.78±1.82CTGF蛋白:11.03±1.12比5.02±1.31,P均<0.01);CTGF的蛋白表达量与转化生长因子(TGF)-β1、纤维结合蛋白(Fn)及ColⅢ的表达量呈正相关(r=0.704、r=0.783及r=0.756,P均<0.01)。结论CTGFmRNA转录和蛋白表达量的增加与LN患者肾小管间质病变程度加重呈正相关。作为TGF-β的下游介质,CTGF可通过促进细胞外基质如FN和ColⅢ等合成,从而在LN患者肾小球硬化及肾小管间质纤维化的     

狼疮性肾炎肾组织CD80与CD86的表达及其意义

目的 研究T淋巴细胞活化分子CD80与CD86在狼疮性肾炎患者肾组织中的表达变化及其与临床指标之间的相关性.方法 肾组织标本来源于2004年12月-2008年10月哈尔滨医科大学附属第一医院住院患者,其中女性44例,男性5例,年龄(28±16)岁.用免疫组织化学法检测狼疮性肾炎及微小病变患者肾组织中的CD80与CD86的表达情况,免疫比浊法检测24 h尿蛋白定量,全自动生化分析仪检测血尿素氮、血肌酐及血浆白蛋白等临床指标.结果 CD80在肾小管上皮细胞、肾间质有阳性表达,在肾小球无表达,而CD86在肾小管上皮细胞、肾间质及肾小球均有表达.CD80与CD86在肾小管间质中的表达水平随着狼疮性肾炎患者肾小管间质病变程度的加重而增强(r=0.574,P<0.001;r=0.534,P<0.001),且CD80的表达与CD86的表达成正相关.CD80与CDB6的表达与患者系统性红斑狼疮疾病活动指数积分(r=0.319,P=0.011;r=0.324,P=0.011)、24 h尿蛋白定量(r=0.424,P=0.003;r:0.408,P=0.004)、肌酐清除率(r=-0.535,P=0.000;r=-0.543,P=0.000)及抗dsDNA抗体滴度(r=0.353,P=0.012;r=0.359,P=0.013)具有明显相关性.结论 CD80与CD86在狼疮性肾炎患者肾组织中的表达水平与肾间质病变具有明显相关性,并且与狼疮性肾炎患者肾活检时的肾功能及活动性明显相关.     

糖原合成酶激酶3β和核因子κB在抗体介导的慢性排斥反应移植肾组织中的表达和意义

目的:探讨糖原合成酶激酶3β(GSK-3β)、核因子κB(NF-κB)和相关炎症性细胞因子在抗体介导的移植肾慢性排斥反应(cABMR)患者肾组织中的表达情况,并分析其与肾间质纤维化/小管萎缩(IF/TA)的关系。方法:用免疫组织化学技术和计算机真彩色图像分析系统半定量检测116例病理诊断符合ABMR的移植肾组织中GSK-3β、NF-κB p65、调节激活正常T细胞表达和分泌的细胞因子(RANTES)和单核细胞趋化蛋白1(MCP-1)的表达,并分析其表达与发生ABMR的移植肾组织IF/TA的关系。以10例肾移植术前零点穿刺肾组织作为对照。结果:在抗体介导的慢性排斥反应肾组织中,GSK-3β、NF-κB p65、RANTES和MCP-1表达水平均较对照组明显增高(P均<0.001),且与IF/TA病理分级呈正相关(r分别为0.884、0.914、0.888和0.868,P<0.001),GSK-3β的表达量同NF-κB p65、RANTES和MCP-1表达亦呈正相关(r分别为0.812、0.804和0.788,P<0.001),随着纤维化程度的加重,患者血清肌酐也逐渐升高(r=0.898,P<0.001)。结论:在ABMR患者移植肾组织中,GSK-3β和NF-κB p65的表达异常增高同移植IF/TA、慢性移植肾失功的发生、发展有关。     

血管钙化大鼠模型Apelin及其受体表达的实验研究

目的观察血管钙化大鼠模型血浆和主动脉组织Apelin及其受体(APJ)的表达。方法选取16只雄性SD大鼠,随机分正常组和钙化组,每组8只。钙化组:08:00肌肉注射维生素D3 3×10^5 U/kg,同时尼古丁25 mg/kg溶于1 mL花生油灌胃,18:00时重复灌胃1次。正常组:类似钙化组操作,但肌肉注射生理盐水和灌胃单纯花生油。4周后取材检测血管钙化程度,用钙离子测试盒、碱性磷酸酶(ALP)试剂盒测定大鼠主动脉钙含量和ALP活性,用酶联免疫吸附法检测大鼠血浆和主动脉组织Apelin含量,用免疫组化法检测大鼠主动脉组织APJ的表达。结果与正常组相比,钙化组中主动脉中膜弹性纤维间可见钙盐沉积,血清和主动脉组织中ALP、钙含量明显升高(P<0.01),而Apelin的表达明显降低(P<0.01),同时,APJ表达亦下调。结论血管钙化大鼠模型Apelin及其受体的表达下调,Apelin/APJ系统可能是新的抑制血管钙化因子。     

肾组织粘附分子及树突状细胞与IgA肾病小管间质病变的关系

目的:观察粘附分子P-选择素与树突状细胞(DC)在IgA肾病(IgAN)患者肾组织中的表达与分布,探讨P-选择素及DC与肾小管间质病变以及肾功能损害的关系.方法:选择经肾活检和临床资料确诊的IgAN患者45例,根据小管间质病变程度分为3组:轻度组29例,中度组10例,重度组6例;10例正常人肾组织作为对照.采用免疫组化法观察IgAN患者肾组织中P-选择素表达;免疫双标记染色与荧光图像分析法,观察CD1a CD80 DC在肾组织中的分布,并探讨DC与患者肾小管间质病变及肾功能损害的关系.结果:①P-选择素在正常肾组织中基本不表达,在IgAN肾组织中以肾小管上皮细胞为主广泛高表达,重度组肾小管间质表达明显强于轻、中度组,且与肾小管间质病变程度轻重显著相关.②正常人肾组织中基本未见CD1a CD80 DC分布,IgAN肾组织中以肾小管间质为主分布明显增多;其在患者肾小管间质的分布于重度组明显高于轻、中度组,亦与肾小管间质病变程度及血肌酐显著相关.此外,CD1a CD80 DC在患者肾小管间质分布与P-选择素表达明显相关.结论:P-选择素尤其DC可能参与了IgAN肾小管间质病变的免疫病理损伤机制,且推测DC肾炎组织迁移聚集可能与P-选择素介导有关.     

系统性红斑狼疮相关血栓性微血管病血管内皮-间充质细胞转分化的研究

目的:探讨系统性红斑狼疮相关血栓性微血管病(SLE-TMA)肾间质血管内皮细胞表型变化及其与血管病变和间质纤维化之间的关系。方法:30例经肾活检明确诊断的SLE-TMA患者,根据血管组织学改变分为急性TMA和慢性TMA,以正常肾组织血管为对照。内皮细胞CD31、血管内皮钙黏蛋白(VE-cadherin)、α平滑肌肌动蛋白(α-SMA)和转化生长因子β(TGF-β)采用间接免疫荧光双重染色定位,免疫组织化学染色和Image-ProPlus 6.0测量上述分子的表达量,以平均光密度表示其表达强度。Aperio图像分析系统测量肾间质纤维化面积。结果:间接免疫荧光双重染色显示正常血管内膜无α-SMA表达,SLE-TMA血管内皮细胞表达α-SMA。与正常对照组相比,急性TMA组血管内皮CD31和VE-cadherin表达降低(P0.05),α-SMA表达则显著增高(P0.01);慢性TMA组内皮细胞CD31、VE-cadherin和TGF-β表达强度均显著低于急性TMA组和正常血管组(P0.01),α-SMA表达更高(P0.01)。肾间质血管α-SMA平均光密度与肾间质纤维化面积呈显著正相关(r=0.439,P=0.015),而CD31平均光密度与肾间质纤维化呈显著负相关(r=-0.458,P=0.011)。结论:SLE-TMA血管内皮细胞正常标记物表达减少而α-SMA表达增加,表明内皮细胞向成纤维细胞表型转变,且表达量的变化与血管病变进展相关;肾血管内皮细胞CD31表达减少和α-SMA增加与肾间质纤维化相关。     

Association of monocyte chemoattractant protein-1 with renal tubular damage in diabetic nephropathy

Monocyte chemoattractant protein-1 (MCP-1), is a chemokine that mediates renal interstitial inflammation, tubular atrophy, and interstitial fibrosis by recruiting monocytes/macrophages into renal tubulointerstitium. Recent studies have demonstrated that protein overload in renal tubular cells up-regulates MCP-1 gene and its protein expression. Therefore, we hypothesized that increased expression of MCP-1 in renal tubuli, probably triggered by an increase in the leakage of plasma protein from glomerular capillary to tubular fluid, may contribute to renal tubular damage and accelerate the progression of diabetic nephropathy. To test this hypothesis, we examined urinary excretion levels of MCP-1 and N-acetylglucosaminidase (NAG), a sensitive marker of renal tubular damage, in Japanese Type II diabetic patients with normoalbuminuria (n=29), microalbuminuria (n=25), and macroalbuminuria (n=18). The median urinary excretion level of MCP-1 in patients with macroalbuminuria (394.4 ng/g creatinine) was significantly elevated compared to the levels in patients with normoalbuminuria and microalbuminuria (159.6 and 193.9 ng/g creatinine, respectively). Furthermore, the urinary MCP-1 excretion level was positively correlated with urinary excretion levels of albumin (r=.816, P<.001) and NAG (r=.569, P<.001) in all subjects. These results suggest that MCP-1 is produced in renal tubular cells and released into urine in proportion to the degree of proteinuria (albuminuria), and that increased MCP-1 expression in renal tubuli contributes to renal tubular damage. Therefore, we conclude that heavy proteinuria itself may accelerate the progression of diabetic nephropathy by increasing the MCP-1 expression in renal tubuli.     

Low plasma apelin levels in newly diagnosed type 2 diabetes mellitus.

OBJECTIVE: To investigate blood apelin concentrations in patients with newly diagnosed and untreated type 2 diabetes mellitus (T2DM) who had no additional disorder and to investigate the association of apelin with adiponectin, body mass indexes (BMI) and insulin sensitivity. METHODS: Forty patients with T2DM and 40 healthy controls were enrolled. Apelin levels were measured along with BMI, lipids, glucose, insulin and adiponectin levels, and HOMA-IR indexes. Age, sex and BMI were similar in the two groups. RESULTS: Plasma apelin and adiponectin levels were significantly lower in the diabetic group compared to controls (p<0.001, for both). Insulin levels and HOMA indexes were significantly higher in patients with T2DM (p<0.001 and p=0.001, respectively). Apelin levels were negatively correlated with age (r=-0.315, p=0.006), fasting blood glucose (r=-0.556, p<0.001) and HOMA indexes (r=-0.411, p=0.001), and positively correlated with plasma adiponectin levels (r=0.593, p<0.001). Plasma adiponectin was negatively correlated to plasma insulin (r=-0.379, p=0.001), fasting glucose (r=-0.604, p<0.001), HOMA-IR (r=-0.559, p<0.001) and BMI (=-0.229, p=0.04). CONCLUSIONS: Plasma apelin is reduced in newly diagnosed and untreated patients with T2DM having no confounders. Regulation of circulating apelin and adiponectin seems to be in the same manner in patients with T2DM. Dysregulation of apelin might be involved in the mechanism of establishment of overt diabetes mellitus as well as associated atherosclerotic complications.     

Evaluation of Fibrosis Markers: Apelin and Transforming Growth Factor‐β1 in Autosomal Dominant Polycystic Kidney Disease Patients

Renal interstitial fibrosis is an important pathological feature of autosomal dominant polycystic kidney disease (ADPKD), which progressively develops to end‐stage renal disease (ESRD). It has been shown that apelin and transforming growth factor‐β1 (TGF‐β1) play important roles in the renal fibrosis process. The aim of the present study is to evaluate the relationship of these fibrosis markers and ADPKD. Forty‐five patients with ADPKD and 28 healthy controls were studied cross‐sectionally. Estimated glomerular filtration rate (eGFR), apelin, TGF‐β1 were measured in all participants, using conventional methods. Apelin levels were lower (1.2 ± 0.9 ng/mL vs. 2.5 ± 1.3 ng/mL, P < 0.001), while TGF‐β1 levels were higher in the patient group according to healthy controls (466.5 ± 200.5 ng/L vs. 367.1 ± 163.45 ng/L, P = 0.031), respectively. Apelin was negatively correlated with TGF‐β1 and highly sensitive C‐reactive protein (hs‐CRP); and positively correlated with eGFR. In all subjects, eGFR was independently predicted by TGF‐β1 and apelin. Apelin and TGF‐β1 may be used as biomarkers of renal fibrosis that is an important pathological feature of ADPKD, which progressively develops to ESRD in ADPKD patients.     

Plasma concentrations of the novel peptide apelin are decreased in patients with chronic heart failure

BACKGROUND: Apelin, the novel endogenous ligand for the G-protein-coupled receptor APJ, has shown positive inotropic, vasodilatory and diuretic properties in animal studies. Differential expression and synthesis of apelin and APJ receptors have been observed in normal and failing human hearts, suggesting a possible role in cardiovascular homeostasis. Changes in plasma apelin concentrations in relation to heart failure have been described in small studies with conflicting results. Our aim was to evaluate plasma apelin concentrations in a large cohort of patients with chronic heart failure (CHF) across a broad spectrum of disease severity. METHOD AND RESULTS: Plasma apelin concentrations were measured in 202 patients with CHF secondary to left ventricular systolic dysfunction and 22 age-matched controls. Plasma apelin concentrations were significantly lower in patients with CHF, irrespective of NYHA class, ejection fraction or aetiology when compared to age-matched controls (0.85 [0.53-2.04] versus 3.76 [0.85-5.13] ng/ml, p<0.001). Apelin concentrations were correlated with peak VO(2) and right ventricular ejection fraction, but not with age, sex, body mass index, renal function or NT-proBNP concentrations. CONCLUSIONS: Plasma apelin concentrations are decreased in patients with CHF. The Apelin-APJ signaling pathway may be a potentially important mediator in the pathophysiological processes of heart failure and may therefore have potential therapeutic implications.     

高血压患者血浆Apelin与左心室肥厚及颈动脉粥样硬化的关系

目的观察高血压患者血浆Apelin水平变化,探讨其与左心室肥厚和颈动脉粥样硬化的关系。方法选择原发性高血压患者125例,根据超声结果分为心肌肥厚组、内膜中膜增厚组、颈动脉斑块组和单纯高血压组,另选31例经体检筛选的健康者为对照组。采用酶联免疫分析法测定血浆Apelin含量。结果心肌肥厚组血浆Ape-lin含量(616±112ng/L)明显低于对照组(757±176ng/L)和单纯高血压组(715±170ng/L,P<0.001或0.05);并且血浆Apelin含量在内膜中膜增厚组(613±133ng/L)和颈动脉斑块组(592±146ng/L)均显著低于单纯高血压组和对照组(P<0.001或0.05)。相关分析表明,血浆Apelin水平与左心室质量指数、内膜中膜厚度和斑块指数均呈明显负相关(r分别为-0.253、-0.255和-0.246,P均<0.05)。结论血浆Apelin水平可能参与高血压心室重构和动脉硬化的发生与发展过程。     

急性冠状动脉综合征患者血清Apelin表达水平与Gensini评分的相关性研究

目的:探讨急性冠状动脉综合征(ACS)患者血清Apelin表达水平及其与Gensini评分的相关性。方法:75例ACS患者分为不稳定型心绞痛(UA)组28例,急性非ST段抬高型心肌梗死(NSTEMI)组11例,急性ST段抬高型心肌梗死(STEMI)组36例,另取13例冠状动脉造影正常者作为对照组。采用Elisa法检测各组血清Apelin表达水平并进行比较,冠状动脉病变程度评分采用Gensini评分系统,分析Apelin表达水平与Gensini评分的关系。结果:Apelin水平从高到低依次为:对照组[(346.38±61.93)ng/L]、UA组[(231.37±67.28)ng/L]、NSTEMI组[(146.59±73.77)ng/L]和STEMI组[(93.46±42.40)ng/L],4组间两两比较均差异有统计学意义(均P<0.001)。相关性检验显示,Apelin表达水平与Gensini评分成负相关(r=-0.426,P<0.001)。结论:血清Apelin水平可能参与了ACS的病理生理过程,其水平越低,冠状动脉病变程度越严重。     

尿视黄醇结合蛋白、N-乙酰-β-D-氨基葡萄糖苷酶及尿蛋白检测在IgA肾病患者肾小管间质损害中的临床意义

目的 探讨尿视黄醇结合蛋白（RBP）、N-乙酰-β-D-氨基葡萄糖苷酶（NAG）及24小时尿蛋白定量（UPE）等指标判断IgA肾病（IgAN）患者肾小管间质损害程度的临床意义.方法 收集我院2010年5月～2013年2月114例住院IgAN患者的临床及病理资料,依据Lee氏病理分级系统将患者分为Lee I～Ⅱ级27例（A组）、LeeⅢ级46例（B组）和LeeⅣ～V级41例（C组）,分析不同分级IgAN肾小管间质病变情况与尿RBP、NAG、UPE等指标之间的相关性.结果 各组间血红蛋白（Hb）、白蛋白（ALB）、前白蛋白（pre-ALB）、血肌酐（SCr）、尿素氮（BUN）、总胆固醇（TC）、UPE、尿RBP及NAG等指标比较差异有统计学意义（P＜0.01）,镜下血尿及高血压的发生率随病理程度加重而上升（P＜0.01）,肾小管萎缩、肾间质炎细胞浸润、肾间质纤维化及动脉硬化在各组间比较差异均有统计学意义（P＜0.01）,相关性分析显示尿RBP、NAG与肾小管萎缩、肾间质炎症细胞浸润、肾间质纤维化及动脉硬化程度呈正相关;UPE与肾小管萎缩程度呈负相关（r=-0.213,P＜0.05）,尿RBP、NAG水平与eGFR呈负相关.结论 IgAN患者高血压及血尿发生率、Hb、ALB、TC、肾功能、RBP、NAG、UPE等指标与肾脏病理损伤程度有关,尿RBP、NAG及UPE联合检测对判断肾小管病理损伤程度及肾功能有临床意义.     

系统性红斑狼疮患者血浆骨桥蛋白水平与疾病活动性及脏器损害的相关性研究

目的 检测系统性红斑狼疮(SLE)患者血浆中骨桥蛋白(OPN)的水平,分析其与SLE活动性及脏器损害间的关系.方法 选择68例SLE患者和36名健康体检者,采用酶联免疫吸附试验(ELISA)检测其血浆中的OPN水平.记录采血时患者的系统性红斑狼疮疾病活动指数(SLEDAI)、实验室指标等.结果 SLE患者OPN血浆水平明显高于正常对照组[(4.5±2.0)ng/ml与(1.6±0.7)ng/ml,P＜0.01 ].SLE疾病活动组高于非活动组[(5.3±2.0)ng/ml与(3.4±1.3)ng/ml,P＜0.01];SLE患者伴有肾脏损害组高于无肾脏损害组[(5.8±2.1)ng/ml与(3.5±1.3)ng/ml,P＜0.01],有肺间质病变、胃肠道病变和心包炎的高于无脏器损害[(4.8±1.2)、(6.3±1.4)、(5.4±2.6)ng/ml与(3.5+1.3)ng/ml,P＜0.05],抗心磷脂抗体阳性患者OPN水平高于抗心磷脂抗体阴性患者[(5.3±2.4)ng/ml与(4.2±1.7)ng/ml,P＜0.05].OPN血浆水平与SLEDAI呈正相关(r=0.523,P＜0.01),与尿蛋白定量(24 h)呈正相关r=0.403,P=0.001),与补体C3呈负相关r=-0.398,P=0.001),与红细胞沉降率(ESR)、抗dsDNA抗体、抗Sm抗体、IgG、IgA、IgM、球蛋白及关节炎等无相关性(P＞0.05) .结论 OPN可能参与SLE的发病,临床上可作为疾病活动及脏器损伤的观察指标.     

血清Apelin-13、可溶性血栓调节蛋白、锁链素对急性肺栓塞患者病情及预后的评估价值

目的 探究血清脂肪细胞因子13(Apelin-13)、可溶性血栓调节蛋白(sTM)、锁链素(DES)对急性肺栓塞(APE)患者病情及预后的评估价值.方法 选取我院2017年10月～2019年8月APE患者118例作为观察组,另选取同期健康体检者115例作为对照组.于两组入院时检测血清Apelin-13、sTM、DES水...