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   大连医科大学学报  2022, Vol. 44 Issue (3): 218-223      DOI: 10.11724/jdmu.2022.03.06
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微炎症与维持性血液透析患者主动脉弓钙化的相关性研究
于平1,2, 邹春波2    
1. 大连医科大学 研究生院, 辽宁 大连 116044;
2. 泰州市人民医院 肾内科, 江苏 泰州 225300
摘要目的 了解维持性血液透析(maintenance hemodialysis, MHD)患者主动脉弓钙化发生情况, 分析微炎症与MHD患者主动脉弓钙化的相关性。方法 选取2018年10月至2020年12月在泰州市人民医院血液净化中心进行规律血液透析的MHD患者71例, 收集患者的一般临床资料、临床生化结果。采用酶联免疫吸附法(enzyme linked immunosorbent assay, ELISA)检测白介素-37(interleukin-37, IL-37)。胸部X线计算主动脉弓钙化评分, 依据评分分为无钙化/轻度钙化组30例(42%)和中重度钙化41例(58%)两组。比较两组患者的一般临床资料、临床生化结果及IL-37;采用Spearman法分析钙化程度与各指标之间的相关性; logistic回归分析钙化的影响因素; ROC曲线评估血小板/淋巴细胞计数(platelet to lymphocyte ratio, PLR)对于主动脉弓中重度钙化的敏感性及特异性。结果 中重度钙化组年龄、透析年限、矫正钙均高于无钙化/轻度钙化组, 差异均有统计学意义(P<0.05)。生化指标: 中重度钙化组中性粒细胞计数/淋巴细胞计数(neutrophil to lymphocyte ratio, NLR)、PLR、IL-37均高于无钙化/轻度钙化组, 活性维生素D、非含钙磷结合剂均低于无钙化/轻度钙化组, 差异均有统计学意义(P<0.05)。血管钙化程度与IL-37、NLR、PLR、年龄、矫正钙、透析年限呈正相关(均P<0.05), 与活性维生素D、非含钙磷结合剂呈负相关(均P<0.05)。二元多因素logistic回归分析提示: 透析年限、高PLR是MHD患者主动脉弓钙化发生的独立危险因素。利用ROC曲线分析PLR预测中重度主动脉弓钙化, 其中PLR敏感性为85.4%, 最佳截断值为90.305, 曲线下面积为0.698(95%CI为0.572~0.825, P<0.05)。结论 MHD患者普遍存在主动脉弓钙化, 透析年限、高PLR是MHD患者主动脉弓钙化独立危险因素, 钙化程度与IL-37、NLR、PLR呈正相关, PLR对于MHD患者主动脉弓钙化具有良好的预测价值。
关键词维持性血液透析    血小板/淋巴细胞计数比值    主动脉弓钙化    微炎症    
Correlation between microinflammation and aortic arch calcification in maintenance hemodialysis patients
YU Ping1,2, ZOU Chunbo2    
1. Graduate School, Dalian Medical University, Dalian 116044, China;
2. Department of Nephrology, Taizhou People's Hospital, Taizhou 225300, China
Abstract: Objective To understand the incidence of aortic arch calcification in patients with Maintenance hemodialysis (MHD) and the correlation between microinflammation and aortic arch calcification in MHD patients. Methods Seventy-one MHD patients, who met the inclusion criteria and underwent regular hemodialysis in Taizhou People's Hospital Blood Purification Center from October 2018 to December 2020, were selected. General clinical data and clinical biochemical results of the patients were collected. IL-37 was detected by enzyme linked immunosorbent assay. Aortic arch calcification score was calculated by chest X-ray and divided into two groups according to the score: 30 patients (42%) had no-calcification/mild calcification and 41 patients (58%) had moderate-to-severe calcification. The general clinical data, clinical biochemical results and IL-37 were compared between the two groups. Spearman method was used to analyze the correlation between the degree of calcification and each index. The influencing factors of calcification were analyzed by logistic regression. ROC curves were used to assess the sensitivity and specificity of PLR for moderate and severe aortic arch calcification. Results The age, dialysis years and corrected calcium of moderate-to-severe calcification group were higher than those of no-calcification/mild calcification group (P < 0.05). Biochemical indexes were as follows: NLR, PLR and IL-37 in moderate-to-severe calcification group were higher than those in no-calcification/mild calcification group, while active vitamin D and non-calcium-phosphorus binding agent were lower than those in no-calcification/mild calcification group (P < 0.05). The degree of vascular calcification was positively correlated with IL-37, NLR, PLR, age, corrected calcium and dialysis years (all P < 0.05), and negatively correlated with active vitamin D and non-calcium-phosphorus binders (all P < 0.05). Binary multiple Logistic regression analysis suggested that dialysis years and high PLR were independent risk factors for aortic arch calcification in MHD patients. PLR was used to predict moderate-to-severe aortic arch calcification using ROC curve analysis. The sensitivity of PLR was 85.4%, the optimal cut-off value was 90.305, and the area under the curve was 0.698 (95%CI was 0.572-0.825, P < 0.05). Conclusion Aortic arch calcification is common in MHD patients. Dialysis years and high PLR are independent risk factors for aortic arch calcification in MHD patients. The degree of calcification is positively correlated with IL-37, NRL and PLR, and PLR has good predictive value for aortic arch calcification in MHD patients.
Keywords: maintenance hemodialysis    platelet-to-lymphocyte ratio    calcification of the aortic arch    microinflammation    

近年来,随着糖尿病、高血压等代谢性疾病发病率不断攀升以及人口老龄化的影响,慢性肾脏病在全球发病率高达10%[1],在我国发病率高达10.8%[2]。慢性肾脏病发展至终末期肾脏疾病(end stage renal disease,ESRD)患者数量逐年上升。截止至2021年,我国有超过1.3亿慢性肾脏病患者,其中需要接受维持性透析(maintenance hemodialysis,MHD)治疗的ESRD患者大约超过100万人[3]。MHD患者血管钙化很常见,钙化通常发生在冠状动脉、主动脉弓、腹主动脉、心脏瓣膜等多个部位,是心血管疾病独立危险因素[4],因此明确MHD患者主动脉弓钙化的相关风险因素尤为重要。MHD患者持续存在微炎症状态,通过多种途径参与调控血管钙化的发生,既往研究表明微炎症指标血小板/淋巴细胞计数(platelet to lymphocyte ratio,PLR)、中性粒细胞计数/淋巴细胞计数(neutrophil to lymphocyte ratio,NLR)、白介素-37(interleukin-37,IL-37)与心血管疾病冠状动脉钙化、瓣膜钙化有关[5-7],因此上述指标可能参与MHD患者主动脉弓钙化。本文旨在通过测定MHD患者血液微炎症指标PLR、NLR、IL-37,分析上述指标与MHD患者主动脉弓钙化相关关系,寻找防治主动脉弓钙化新靶标。

1 资料与方法 1.1 研究对象

选取2018年10月至2020年12月在泰州市人民医院血液净化中心维持性血液净化患者71例。其中男性37例(52%), 女性34例(48%),年龄(56±10)岁,原发病为慢性肾小球肾炎51例(72%)、糖尿病肾病6例(8%)、多囊肾5例(7%)、其他疾病9例(13%)。其中根据胸部X线评分,将MHD患者分为无钙化/轻度钙化组30例(42%)和中重度钙化组41例(58%)。

纳入标准:入选患者年龄>18岁;规律维持血液透析时间>6个月。排除标准:入组前1个月内有过感染(临床表现为发热、咳嗽、恶心、呕吐、腹泻等)或使用过抗生素;恶性肿瘤;血液系统疾病:粒细胞缺乏症、原发性血小板减少性紫癜;甲状腺手术切除史;妊娠期或者哺乳期妇女。透析方案:每周规律血液透析3次,每次4 h,透析通路为颈内静脉通路或自体动静脉内瘘。研究经过泰州市人民医院伦理委员会批准(批件号:KY 2020-153-01)。

1.2 研究方法 1.2.1 基本信息采集

收集入选者一般临床资料:性别、年龄、透析龄、原发病、血压值以及服用药物情况;通过LIS以及HIS系统收集患者拍摄肺部X线1周内所检测的生化检验结果:血红蛋白、血清白蛋白、碱性磷酸酶、血清钙、血清磷、血清镁、中性粒细胞计数、淋巴细胞计数、血小板计数、血清甘油三酯、血清总胆固醇、高密度脂蛋白、低密度脂蛋白以及通过心脏彩超影像结果:左室射血分数、左心房内径等;根据血清白蛋白计算血清钙水平:校正钙(mmol/L)=血清钙(mmol/L)+0.02×[40-白蛋白(g/L)],NLR=中性粒细胞计数/淋巴细胞计数,PLR=血小板/淋巴细胞计数。

1.2.2 血液标本采集

收集患者清晨透析前静脉血3 mL,室温下静置40 min,放置在低温高速离心机3 000 r/min,离心30 min,将离心后的血清转移到1.5 mL的EP管中,标记好患者信息并编号,保存至-80 ℃冰箱内留用,采用酶联免疫吸附法(enzyme linked immunosorbent assay, ELISA) 检测IL-37。

1.2.3 血管钙化评估

由两位高年资放射科医生盲审,通过患者胸部X线,评估主动脉弓钙化程度,0级:无钙化;1级(轻度):点状或薄片状钙化;2级(中度):一个或多个区域呈现钙化增厚增密;3级(重度):呈现圆周样钙化。

1.3 统计学方法

采用SPSS 25.0进行统计分析。计数资料以频数和百分比表示,呈正态分布的计量资料采用均数±标准差(x±s)表示, 非正态分布的计量资料用中位数和四分位数间距[M(P25P75)]表示。正态分布资料两组间比较采用t检验, 非正态分布资料采取Wilcoxon秩和检验, 分类资料采取χ2检验。采用Spearman法分析钙化程度与各指标之间的相关性。通过logistic回归分析钙化的影响因素。采用ROC曲线分析各指标对于钙化诊断的准确性。P<0.05为差异有统计学意义。

2 结果 2.1 两组相关指标比较分析

本研究纳入无钙化/轻度钙化组年龄(53±9)岁。中重度钙化组年龄(59±10)岁,中重度钙化组年龄、透析年限均高于无钙化/轻度钙化组(均P<0.05);服用活性维生素D比例、服用非含钙磷结合剂比例均低于无钙化/轻度钙化组(均P<0.05)。生化指标:中重度钙化组矫正钙、NRL、PLR、IL-37均高于无钙化/轻度钙化组(均P<0.05),其余生化指标差异无统计学意义(均P>0.05)。见表 1

表 1 两组患者一般情况比较 Tab 1 Comparison of general data between the two groups
项目 无钙化/轻度钙化组(n=30) 中重度钙化组(n=41) t/z/χ2 P
年龄/岁,x±s 53±9 59±10 -2.572 0.012
透析年限/年,M(P25P75) 3(2, 7) 5(3, 10) -2.765 0.006
男性,n(%) 14(46.7) 23(56.1) 0.617 0.432
脉压差/mmHg,M(P25P75) 50(41, 60) 50(40, 60) -0.661 0.508
高血压病程/年,M(P25P75) 10(4, 10) 10(3, 13) -0.932 0.351
原发病,n(%)
  慢性肾小球肾炎 20(66.7) 31(75.6) 3.702 0.054
  糖尿病肾病 2(6.7) 4(9.8) 0.681
  多囊肾 2(6.7) 3(7.3) 1.000
  其他疾病 6(20.0) 3(7.3) 0.493
ACEI/ARB,n(%) 7(23.3) 5(12.2) 1.530 0.216
β受体阻滞剂,n(%) 12(40.0) 12(29.3) 0.892 0.345
CCB,n(%) 21(70.0) 33(80.5) 1.046 0.306
活性维生素D,n(%) 14(46.7) 8(19.5) 5.973 0.015
非含钙磷结合剂,n(%) 16(53.3) 11(26.8) 5.164 0.023
左心房内径/mm,M(P25P75) 40(37, 44) 41(41, 44) -1.340 0.180
左心室内径/mm,x±s 50.793±6.737 50.626±6.476 0.106 0.916
射血分数/%,M(P25P75) 66(62, 71) 65(64, 68) -0.509 0.611
血红蛋白/(g/L),M(P25P75) 100(93, 108) 101(86, 117) -0.099 0.921
碱性磷酸酶/(U/L),M(P25P75) 84(62, 99) 89(75, 117) -1.811 0.070
校正钙/(mmol/L),M(P25P75) 2.16(1.91, 2.36) 2.38(2.26, 2.46) -2.670 0.006
磷/(mmol/L),x±s 1.957±0.443 1.931±0.505 0.199 0.843
镁/(mmol/L),M(P25P75) 1.05(0.92, 1.13) 1.05(0.95, 1.09) -0.448 0.654
前白蛋白/(mg/L),M(P25P75) 357(311, 411) 348(275, 389) -1.543 0.123
甘油三酯/(mmol/L),M(P25P75) 1.69(1.35, 2.05) 1.57(1.02, 2.17) -0.676 0.499
总胆固醇/(mmol/L),M(P25P75) 3.74(3.11, 4.64) 3.52(3.16, 4.22) -0.625 0.514
高密度脂蛋白/(mmol/L),x±s 0.940±0.194 0.927±0.215 0.262 0.794
低密度脂蛋白/(mmol/L),M(P25P75) 2.27(1.78, 2.50) 2.24(1.89, 2.53) -0.700 0.484
NRL,M(P25P75) 2.88(2.36, 3.59) 4.16(3.42, 6.50) -1.343 0.002
PLR,M(P25P75) 93.04(63.59, 160) 155.56(103.95, 212.12) -2.840 0.005
IL-37/(pg/mL),M(P25P75) 8.81(6.93, 10.69) 10.79(8.41, 15.76) -2.514 0.012
注:ACEI/ARB:血管紧张素转换酶抑制剂/血管紧张素受体拮抗剂;CCB:钙离子通道阻滞剂;NLR=中性粒细胞计数/淋巴细胞计数;PLR=血小板/淋巴细胞计数;IL-37:白介素-37。
2.2 血管钙化程度与相关指标相关性分析

血管钙化程度与IL-37、NLR、PLR、年龄、矫正钙、透析年限呈正相关(均P<0.05),与服用活性维生素D比例、服用非含钙磷结合剂比例呈负相关(均P<0.05)。见表 2

表 2 血管钙化与相关指标相关性分析 Tab 2 Correlation analysis of vascular calcification and related indicators
项目 血管钙化程度
r P
IL-37 0.301 0.011
NLR 0.376 0.001
PLR 0.339 0.004
年龄 0.251 0.034
矫正钙 0.330 0.005
透析年限 0.330 0.005
活性维生素D -0.290 0.014
非含钙磷结合剂 -0.270 0.023
注:NLR=中性粒细胞计数/淋巴细胞计数;PLR=血小板/淋巴细胞计数;IL-37:白介素-37。
2.3 主动脉弓钙化的影响因素分析

将差异有统计学意义的单因素纳入二元多因素logistic回归分析提示:透析年限(OR=1.163,P=0.044)、高PLR(OR=1.009,P=0.042)是MHD患者中重度主动脉弓钙化发生的独立危险因素。见表 3

表 3 主动脉弓钙化的logistic回归分析 Tab 3 Logistic regression analysis of aortic arch calcification
项目 B Wald OR 95%CI P
IL-37 0.042 1.314 1.043 0.971~1.120 0.252
透析年限 0.151 4.048 1.163 1.004~1.348 0.044
非含钙磷结合剂 0.942 2.569 2.565 0.811~8.115 0.109
NLR 0 0 1 0.874~1.145 1.000
PLR 0.009 4.133 1.009 1.000~1.018 0.042
注:NLR=中性粒细胞计数/淋巴细胞计数;PLR=血小板/淋巴细胞计数;IL-37:白介素-37。
2.4 PLR对主动脉弓钙化的评估价值

利用ROC曲线分析PLR预测中重度主动脉弓钙化,其中PLR敏感性为85.4%,最佳截断值为90.305,曲线下面积为0.698(95%CI为0.572~0.825,P<0.05)。见图 1

图 1 PLR预测中重度主动脉弓钙化的ROC曲线分析 Fig 1 ROC curve analysis of PLR prediction of moderate-to-severe aortic arch calcification
3 讨论

慢性肾脏病患者血管钙化是导致心血管疾病(cardiovascular disease,CVD)等并发症的风险因素[8]。MHD患者合并CVD死亡率较一般人群高10~30倍[9]。本研究71例血液透析患者主动脉弓中重度钙化发生率为58%,提示MHD患者主动脉弓钙化发病率高。二元多因素logistic回归分析结果提示:透析年限、PLR是主动脉弓钙化发生的独立危险因素,随着透析年限增加,血管钙化程度加重,这与周晓玲等的研究一致[10]。有研究报道对于主动脉弓钙化的评估与随访,有助于对于维持性血液透析患者的死亡风险进行分层[11]。本研究通过胸部X线评估患者主动脉弓钙化发生情况,以及影响因素,对于减少患者心血管疾病死亡风险具有一定意义。

MHD患者存在氧化应激状态,促进炎症介质的释放,导致糖基化终产物的增多[12],引起微炎症状态的发生。既往研究表明氧化应激与微炎症状态二者相互促进,加速血管钙化发生[13]。微炎症状态的激活主要表现为单核巨噬细胞系统激活、白细胞介素、肿瘤坏死因子α、C反应蛋白(CRP)等释放。本研究表明钙化程度与年龄、矫正血钙、透析年限呈正相关(P<0.05),与非含钙磷结合剂、活性维生素D呈负相关(P<0.05)。随着年龄、透析年限增加,应更加注意患者血管钙化的发生。既往研究表明补充外源性活性维生素D,可以促进MHD患者血管内皮功能恢复,降低机体炎症反应进而进一步减轻患者动脉钙化程度[14]。近期荟萃分析表明与非含钙磷结合剂相比,长期大量服用含钙磷结合剂将导致心血管钙化、心血管疾病死亡等不良事件发生[15]。同时本研究还表明钙化程度与IL-37、NRL、PLR呈正相关(P<0.05),提示IL-37、NRL、PLR对于主动脉弓钙化诊断具有一定价值。IL-37是具有抗炎作用的细胞因子,为IL-1家族成员之一,通过调节巨噬细胞极化和脂质代谢将细胞因子表达从促炎症转变为抗炎作用[16]。本研究表明中重度钙化组中IL-37高于无钙化/轻度钙化组,差异具有统计学意义(P<0.05),但是缺乏IL-37抗炎直接证据。Chai M等[17]通过载脂蛋白E缺陷型糖尿病小鼠体外实验证实IL-37治疗可导致血清中骨保护素浓度升高,IL-37不仅可以减轻动脉粥样硬化,还可以减轻血管钙化。本研究多因素回归分析提示IL-37不是主动脉弓钙化的保护因素,差异无统计学意义,考虑与样本单一性及地区差异有关,IL-37与主动脉弓钙化的关系仍需进一步深入研究。

既往研究认为NLR为传统炎症标记物,与心血管疾病如心力衰竭、冠状动脉疾病有关[18]。中性粒细胞可以释放各种炎症介质和细胞因子,导致慢性微炎症状态,慢性炎症会增加血小板计数,淋巴细胞凋亡介导炎症介质产生,加速血管钙化产生[19]。健康成人NLR值介于0.78和3.53之间。本研究中重度钙化组中位NLR数值4.16(3.42,6.50),明显高于正常健康成人。本研究提示中重度钙化组NLR、PLR明显高于轻度/无钙化组,可能是促进主动脉弓钙化的因素。有研究认为PLR是非特异性炎症标记物,PLR水平升高可能与血小板过度激活和淋巴细胞减少有关。既往研究发现MHD患者相对血小板增多与心血管疾病死亡风险较高相关[20]。本研究显示高PLR与主动脉弓钙化有关,是MHD患者主动脉弓钙化发生的相对危险因素,ROC曲线结果显示PLR曲线下面积0.698,最佳截断值:90.305,敏感性为85.4%,特异性为50%。当MHD患者PLR值>90.305时,应高度重视对于患者主动脉弓钙化的评估,及时发现问题并干预钙化的相关危险因素。考虑到主动脉弓钙化为心血管不良事件的危险因素[21],PLR是一种简单、应用广泛、廉价且容易获得的炎症标志物,PLR联合X线检查可能成为筛查MHD患者主动脉弓钙化的可靠方法。

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文章信息

于平, 邹春波
YU Ping, ZOU Chunbo
微炎症与维持性血液透析患者主动脉弓钙化的相关性研究
Correlation between microinflammation and aortic arch calcification in maintenance hemodialysis patients
大连医科大学学报, 2022, 44(3): 218-223.
Journal of Dalian Medical University, 2022, 44(3): 218-223.
通信作者
邹春波, 教授。E-mail: shilz123@yeah.net.

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