2. 复旦大学附属中山医院肾内科, 上海 200032
2. Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai 200032, China
慢性肾脏病(chronic kidney disease, CKD)已成为全球性公共卫生问题,患病率逐年上升,可导致肾衰竭、心血管疾病(cardiovascular diseases, CVD)和过早死亡等不良预后[1-2]。左心室肥厚(left ventricular hypertrophy, LVH)在CKD患者中高发,且与不良预后相关[3-5]。神经内分泌失调、尿毒症毒素潴留、炎症、容量过负荷等均可导致CKD患者心脏重构或LVH发生[6-8]。左心室构型可分为正常构型(normal geometry, NG)、向心性重构(concentric remodeling, CR)、向心性LVH(concentric LVH, cLVH)和离心性LVH(eccentric LVH, eLVH)。不同的左心室构型影响疾病危险分层和预后评估[9-11]。
生长刺激表达基因2蛋白(growth stimulation expressed gene 2 protein, ST2)是白细胞介素1(interleukin-1, IL-1)受体家族成员,与多种心血管疾病的发生相关。ST2在体内主要有2种形式:跨膜型(membrane bound ST2,ST2L)和可溶性(soluble ST2, sST2)。IL-33是一种组织源性核细胞因子,是ST2L的功能配体。IL-33与ST2L结合可减少心肌纤维化、肥大和心肌细胞凋亡,发挥保护心脏的作用。而血液中的sST2可作为IL-33的诱饵受体,与ST2L竞争结合IL-33,中断IL-33/ST2L信号通路,促使心肌细胞纤维化[12-14]。sST2可作为不同心血管疾病的预后标志物,尤其可应用于心衰患者[15-20]。另有研究[21-22]显示,接受血液透析(hemodialysis, HD)治疗的终末期肾病(end-stage kidney disease, ESKD)患者sST2升高提示预后不良。
但是,目前IL-33/ST2通路在心脏重构中的作用,及sST2与左心室重构的关系尚有争议[23-25],尤其在非透析CKD(non-dialysis-dependent CKD,NDD-CKD)人群中,sST2与左心室构型之间的关系尚未明确。因此,本研究旨在分析NDD-CKD患者中sST2及传统心脏标志物与左心室构型的相关性。
1 资料与方法 1.1 一般资料连续收集2019年8月至2020年12月在复旦大学附属中山医院肾内科治疗的NDD-CKD患者。纳入标准:(1)年龄≥18岁;(2)CKD诊断符合改善全球肾脏病预后组织(Kidney Disease: Improving Global Outcomes, KDIGO)临床实践指南[26]标准,即出现肾脏损伤或估算肾小球滤过率(eGFR)<60 mL·min﹣1·(1.73 m2)﹣1,且持续时间超过3个月。eGFR采用慢性肾脏疾病流行病学协作公式(chronic kidney disease epidemiology collaboration, CKD-EPI)[26]计算。排除标准:(1)1个月内有感染史或活动性感染;(2)使用糖皮质激素或免疫抑制剂;(3)先天性心脏病;(4)心脏瓣膜病;(5)既往心肌梗死史;(6)急性肾损伤;(7)透析患者;(8)肾移植史。本研究符合《赫尔辛基宣言》,并获得复旦大学附属中山医院伦理委员会批准(B2014-026),所有患者均签署知情同意书。
1.2 临床及实验室指标收集患者入院时基线资料,包括年龄、性别、身高、体质量、收缩压和舒张压、体质量指数(body mass index, BMI),既往史、合并症、用药史。CKD分期采用KDIGO临床实践指南[26]标准。所有患者均于入院后采集清晨空腹时的静脉血样本,测定血红蛋白、血清白蛋白、肌酐、甲状旁腺激素、N端脑钠肽前体(N-terminal pro-B-type natriuretic peptide, NT-proBNP)和高敏心肌肌钙蛋白T(high-sensitivity cardiac troponin T, hs-cTnT)水平。通过酶联免疫吸附法(Presage® ST2 Assay, Critical Diagnostics公司, 美国)检测sST2水平。
1.3 超声心动图参数及左心室构型所有患者入院后进行经胸超声心动图检查,由2位高年资主治医师用彩色多普勒超声心动图仪(型号:iE33,飞利浦)进行检查。受检者取左侧卧位,根据美国超声心动图学会指南[27]推荐的方法,测量主动脉根部直径(aortic root diameter,AOD)、左心房内径(left atrial diameter,LAD)、左心室舒张末期内径(left ventricular end-diastolic diameter,LVEDD)、左心室收缩末期内径(left ventricular end-systolic diameter,LVESD)、舒张末期后壁厚度(posterior wall thickness at end-diastole,PWT)、舒张末期室间隔厚度(interventricular septum thickness at end-diastole,IVST)、左心室射血分数(left ventricularejection fraction,LVEF)。左心室质量(left ventricular mass, LVM)=0.8×[1.04×(IVST+LVEDD+LVPWT)3-LVEDD3]+0.6。LVMI=LVM/身高2.7;LVH:男性LVMI>50 g/m2.7,女性LVMI>47 g/m2.7。相对室壁厚度(relative wall thickness, RWT)=(IVST+PWT)/LVEDD,正常值<0.42。根据LVMI和RWT,左心室构型分为4型:NG为LVMI和RWT均正常;CR为LVMI正常、RWT大于正常值;cLVH为LVMI和RWT均大于正常值;eLVH为LVMI大于正常值,RWT正常。
1.4 统计学处理使用RStudio(v1.3.1093)进行统计分析。符合正态分布的计量资料以x±s表示,组间比较采用t检验或单因素方差分析;非正态分布的计量资料以M(P25,P75)表示,组间比较采用Kruskal-Wallis H检验。计数资料以n(%)表示,组间比较采用χ2检验或Fisher精确检验。采用ROC曲线分析各心脏标志物对LVH的预测效能。将NT-proBNP、hs-cTnT和sST2进行对数转换,采用Tukey事后检验分析其在各左心构型患者间的差异。采用多元线性回归分析心脏标志物与心脏结构参数之间的相关性。检验水准(α)为0.05。
2 结果 2.1 一般临床特征及实验室指标共纳入652例患者,其中男性425例、女性227例,年龄54(39,64)岁,中位eGFR为42 mL·min﹣1·(1.73 m2)﹣1;高血压470例(72.1%)、糖尿病163例(25.0%);LVH检出218例(33.4%),最常见构型为NG(288例,44.2%)。结果(表 1)显示:各左心室构型组间患者年龄、身高、BMI、收缩压,血红蛋白、血清肌酐、eGFR及甲状旁腺素水平,合并症差异均有统计学意义(P<0.01);NG组高血压和糖尿病患者比例均最低。
指标 | NG(n=288) | CR(n=146) | cLVH(n=143) | eLVH(n=75) | P值 |
年龄/岁 | 44(34, 56.3) | 57(46, 66) | 61(47, 68) | 60(49, 67.5) | <0.001 |
男性n(%) | 179(62.2) | 107(73.3) | 95(66.4) | 44(58.7) | 0.072 |
体质量/kg | 69(59, 77.6) | 69(61, 75.8) | 70(60, 79) | 70(62, 78) | 0.707 |
身高/m | 1.67(1.60, 1.73) | 1.69(1.61, 1.72) | 1.65(1.60, 1.70) | 1.66(1.60, 1.70) | 0.005 |
BMI/(kg·m﹣2) | 24.3(22.0, 27.0) | 24.5(22.1, 26.5) | 25.4(23.1, 27.7) | 25.4(23.3, 27.9) | 0.002 |
收缩压/mmHg | 132(119, 144) | 140(127, 156) | 150(136, 166) | 143(130, 160) | <0.001 |
舒张压/mmHg | 81(74, 90) | 83(76, 91.8) | 85(76, 93) | 79(70, 90) | 0.059 |
sST2/(ng·mL﹣1) | 25.0(19.2, 32.8) | 26.6(20.7, 37.4) | 28.0(22.5, 37.3) | 27.2(18.9, 36.1) | 0.023 |
NT-proBNP/(pg·mL﹣1) | 61.3(33.1, 402) | 107(46.4, 434) | 985(238, 2 303) | 1 096(339, 3 243) | <0.001 |
hs-cTnT/(ng·mL﹣1) | 0.008(0.005, 0.015) | 0.013(0.008, 0.031) | 0.030(0.019, 0.062) | 0.039(0.014, 0.048) | <0.001 |
Hb/(g·L﹣1) | 125(108, 140) | 124(102, 141) | 106(84, 119) | 97(80.5, 113) | <0.001 |
Alb/(g·L﹣1) | 39(33, 42) | 38(31, 41) | 36(31, 39) | 37(33, 40) | 0.579 |
sCr/(μmol·L﹣1) | 110(77, 171) | 127(90.5, 226) | 337(159, 543) | 369(188, 651) | <0.001 |
eGFR/[mL·min﹣1·(1.73 m2)﹣1] | 64(35.8, 96) | 48.5(23.2, 78.8) | 15(9, 39) | 13(7, 31) | <0.001 |
PTH/(pg·mL﹣1) | 39.1(28.2, 57.4) | 46.7(31.4, 77.6) | 78.9(44.5, 204) | 137(55.5, 203) | <0.001 |
合并症n(%) | |||||
高血压 | 147(51.0) | 120(82.2) | 136(95.1) | 67(89.3) | <0.001 |
糖尿病 | 41(14.2) | 55(37.7) | 47(32.9) | 20(26.7) | <0.001 |
用药史n(%) | |||||
ACEI | 8(2.8) | 3(2.1) | 1(0.7) | 3(0.04) | 0.356 |
ARB | 77(26.7) | 48(32.9) | 35(24.5) | 19(25.3) | 0.400 |
ARNI | 0 | 0 | 2(0.01) | 1(0.01) | 0.057 |
α受体阻滞剂 | 3(1.0) | 6(4.1) | 19(13.3) | 9(12.0) | <0.001 |
β受体阻滞剂 | 25(8.7) | 29(19.9) | 55(38.5) | 27(36.0) | <0.001 |
CCB | 92(31.9) | 86(58.9) | 103(72.0) | 54(72.0) | <0.001 |
利尿剂 | 10(3.5) | 4(2.7) | 7(4.9) | 7(9.3) | 0.130 |
MRA | 2(0.7) | 0 | 2(1.4) | 0 | 0.377 |
sGLT2i | 0 | 2(1.4) | 1(4.9) | 1(1.3) | 0.099 |
抗血小板药物 | 8(2.8) | 11(7.5) | 20(14.0) | 5(6.7) | <0.001 |
他汀 | 15(5.2) | 18(12.3) | 21(14.7) | 7(9.3) | 0.005 |
NG:正常构型;CR:向心性重构;cLVH:向心性肥厚;eLVH:离心性肥厚;BMI:体质量指数;sST2:可溶性生长刺激表达基因2蛋白;NT-proBNP:N端脑钠肽前体;hs-cTnT:高敏心肌肌钙蛋白T;Hb:血红蛋白;Alb:白蛋白;sCr:血肌酐;eGFR:估算肾小球滤过率;PTH:甲状旁腺激素;ACEI:血管紧张素转换酶抑制剂;ARB:血管紧张素受体拮抗剂;ARNI:血管紧张素受体脑啡肽酶抑制剂;CCB:钙离子拮抗剂;MRA:醛固酮受体拮抗剂;sGLT2i:钠-葡萄糖协同转运蛋白2抑制剂。 |
患者超声心动图参数见表 2。结果(表 3)显示:LVH检出率随着肾功能恶化而升高,以G5期患者LVH检出率最高(64.3%)。
参数 | NG(n=288) | CR(n=146) | cLVH(n=143) | eLVH(n=75) | 总计(N=652) |
AOD/mm | 32.5±3.24 | 33.7±3.59 | 34.8±3.64 | 34.6±3.88 | 33.5±3.62 |
LAD/mm | 36.2±4.88 | 37.9±4.41 | 42.3±4.63 | 42.9±4.58 | 38.7±5.45 |
LVEDD/mm | 46.9±3.68 | 44.1±3.18 | 49.8±4.55 | 54.1±4.33 | 47.7±4.89 |
LVESD/mm | 29.6±2.55 | 28.4±2.25 | 32.7±4.61 | 36.3±5.67 | 30.8±4.29 |
IVST/mm | 8.81±0.91 | 10.6±1.18 | 12.5±1.31 | 10.5±1.04 | 10.2±1.80 |
PWT/mm | 8.59±0.95 | 9.86±0.96 | 11.6±1.61 | 10.2±0.86 | 9.72±1.63 |
RWT | 0.371±0.028 | 0.466±0.043 | 0.487±0.054 | 0.382±0.027 | 0.419±0.064 |
LVEF/% | 66.4±3.11 | 65.0±2.93 | 62.4±6.83 | 60.6±9.6 | 64.5±5.59 |
LVM/g | 138±31.8 | 155±31.2 | 239±61.9 | 220±48.2 | 173±59.7 |
LVMI/(g·m﹣2.7) | 34.3±6.45 | 38.4±5.96 | 61.2±12.8 | 56.7±8.95 | 43.7±14.3 |
NG:正常构型;CR:向心性重构;cLVH:向心性肥厚;eLVH:离心性肥厚;AOD:主动脉根部直径;LAD:左房内径;LVEDD:左心室舒张末期内径;LVESD:左心室收缩末期内径;IVST:舒张末期室间隔厚度;PWT:舒张末期后壁厚度;RWT:相对室壁厚度;LVEF:左心室射血分数;LVM:左心室质量;LVMI:左心室质量指数。 |
n(%) | |||||||||||||||||||||||||||||
分期 | NG (n=288) | CR (n=146) | cLVH (n=143) | eLVH (n=75) | 总计 | ||||||||||||||||||||||||
G1 | 91(69.5) | 29(22.1) | 9(6.9) | 2(1.5) | 131(20.1) | ||||||||||||||||||||||||
G2 | 68(59.1) | 32(27.8) | 9(7.8) | 6(5.2) | 115(17.6) | ||||||||||||||||||||||||
G3 | 70(44.0) | 41(25.8) | 35(22.0) | 13(8.2) | 159(24.4) | ||||||||||||||||||||||||
G3a | 32(53.3) | 14(23.3) | 11(18.3) | 3(5.0) | 60(9.2) | ||||||||||||||||||||||||
G3b | 38(38.4) | 27(27.3) | 24(24.2) | 10(10.1) | 99(15.2) | ||||||||||||||||||||||||
G4 | 23(30.3) | 19(25) | 20(26.3) | 14(18.4) | 76(11.7) | ||||||||||||||||||||||||
G5 | 36(21.1) | 25(14.6) | 70(40.9) | 40(23.4) | 171(26.2) | ||||||||||||||||||||||||
NG:正常构型;CR:向心性重构;cLVH:向心性肥厚;eLVH:离心性肥厚。 |
结果(图 1)显示:NT-proBNP诊断CKD患者发生LVH的ROC曲线下面积(AUC)为0.832(95%CI 0.800~0.864);hs-cTnT诊断AUC为0.785(95%CI 0.750~0.821),小于NT-proBNP(P<0.001)。sST2诊断AUC为0.544(95%CI 0.497~0.591)。
2.4 各左心室构型及有无LVH组间心脏标志物差异 2.4.1 不同左心室构型组间差异结果(表 1)显示:不同左心室构型组间sST2、NT-proBNP、hs-cTnT差异均有统计学意义(P<0.05)。事后检验(图 2)示:sST2在cLVH与NG间差异有统计学意义(P=0.025);NT-proBNP在CR与NG(P=0.003)、cLVH与NG(P<0.001)、eLVH与NG(P<0.001)、cLVH与CR(P<0.001)、eLVH与CR(P<0.001)组间差异均有统计学意义;hs-cTnT在CR与NG、cLVH与NG、eLVH与NG、cLVH与CR、eLVH与CR组间差异均有统计学意义(P<0.001)。
2.4.2 LVH组与无LVH组间差异事后检验(图 3)显示:相较于无LVH组,LVH组血清hs-cTnT和NT-proBNP升高(P<0.001),sST2升高不明显(P=0.056)。
2.5 心脏标志物与超声心动图参数的相关性多元线性回归分析(表 4)显示:NT-proBNP和hs-cTnT与所有测量的超声心动图参数有一定相关性(P<0.000 1);sST2仅与LAD、IVST、PWT、RWT、LVM和LVMI有一定相关性(P<0.01),与LVM和LVMI相关性更大(P<0.01)。校正年龄、性别、糖尿病、eGFR、血压和BMI等混杂因素后,NT-proBNP和hs-cTnT仍与所有超声心动图参数有一定相关性(P<0.01);sST2与所有超声心动图参数无相关性。进一步校正另外2种心脏标志物后,NT-proBNP、hs-cTnT仍与多个超声心动图参数相关;sST2与LAD及LVMI相关(P<0.01)。
β值(95%CI) | |||||||||||||||||||||||||||||
指标 | LAD | LVEDD | LVESD | IVST | PWT | ||||||||||||||||||||||||
sST2 | |||||||||||||||||||||||||||||
未调整 | 0.50(0.01~0.92)* | 0.33(﹣0.04~0.71) | 0.32(﹣0.01~0.65) | 0.21(0.07~0.34)** | 0.22(0.10~0.35)*** | ||||||||||||||||||||||||
模型1 | 0.09(﹣0.22~0.41) | ﹣0.01(﹣0.33~0.32) | 0.03(﹣0.27~0.32) | 0.06(﹣0.05~0.18) | 0.09(﹣0.02~0.19) | ||||||||||||||||||||||||
模型2 | ﹣0.30(﹣0.60~﹣0.01)* | ﹣0.24(﹣0.56~0.08) | ﹣0.26(﹣0.54~0.02) | ﹣0.05(﹣0.16~0.07) | ﹣0.01(﹣0.12~0.09) | ||||||||||||||||||||||||
NT-proBNP | |||||||||||||||||||||||||||||
未调整 | 2.80(2.44~3.16)*** | 1.79(1.44~2.14)*** | 1.77(1.47~2.08)*** | 0.83(0.71~0.95)*** | 0.73(0.62~0.84)*** | ||||||||||||||||||||||||
模型1 | 2.75(2.26~3.24)*** | 2.02(1.50~2.54)*** | 2.37(1.92~2.83)*** | 0.63(0.45~0.82)*** | 0.63(0.46~0.80)*** | ||||||||||||||||||||||||
模型2 | 2.47(1.92~3.02)*** | 2.24(1.65~2.83)*** | 2.52(2.00~3.04)*** | 0.44(0.24~0.65)*** | 0.48(0.29~0.68)*** | ||||||||||||||||||||||||
hs-cTnT | |||||||||||||||||||||||||||||
未调整 | 3.15(2.81~3.50)*** | 1.81(1.46~2.16)*** | 1.66(1.35~1.96)*** | 1.01(0.89~1.12)*** | 0.84(0.73~0.95)*** | ||||||||||||||||||||||||
模型1 | 1.89(1.37~2.41)*** | 0.68(0.13~1.23)*** | ﹣0.13(﹣0.66~0.40)*** | 0.45(0.24~0.66)*** | 0.56(0.38~0.73)*** | ||||||||||||||||||||||||
模型2 | 0.83(0.27~1.39)** | ﹣0.31(﹣0.9~0.29) | ﹣0.26(﹣0.54~0.02) | ﹣0.04(﹣0.16~0.07)*** | 0.33(0.13~0.53)** | ||||||||||||||||||||||||
指标 | RWT | LVEF | LVM | LVMI | |||||||||||||||||||||||||
sST2 | |||||||||||||||||||||||||||||
未调整 | 0.01(0.002~0.012)** | ﹣0.38(﹣0.81~﹣0.04) | 6.26(1.69~﹣10.83)** | 1.19(0.10~2.29)* | |||||||||||||||||||||||||
模型1 | 0.004(﹣0.000 5~0.009) | ﹣0.11(﹣0.54~0.31) | 0.93(﹣2.69~4.54) | ﹣0.03(﹣0.98~0.92) | |||||||||||||||||||||||||
模型2 | ﹣0.01(﹣0.01~0.03) | 0.32(﹣0.10~0.73) | ﹣3.28(﹣6.71~0.16) | ﹣1.11(﹣2.02~﹣0.20)* | |||||||||||||||||||||||||
NT-proBNP | |||||||||||||||||||||||||||||
未调整 | 0.02(0.01~0.02)*** | ﹣2.04(﹣2.44~﹣1.64)*** | 29.9(25.9~33.9)*** | 7.91(6.99~8.82)*** | |||||||||||||||||||||||||
模型1 | 0.01(0.002~0.02)* | ﹣3.41(﹣4.08~﹣2.74)*** | 29.52(23.9~35.1)*** | 8.28(6.46~10.10)*** | |||||||||||||||||||||||||
模型2 | 0.000 5(﹣0.01~0.01) | ﹣3.46(﹣4.22~﹣2.70)*** | 27.04(20.7~33.4)*** | 7.01(4.97~9.05)*** | |||||||||||||||||||||||||
hs-cTnT | |||||||||||||||||||||||||||||
未调整 | ﹣1.61(﹣2.01~﹣1.20)*** | 32.7(28.9~36.6)*** | 7.52(6.58~8.45)*** | 0.02(0.02~0.03)*** | |||||||||||||||||||||||||
模型1 | 0.02(0.01~0.03)*** | ﹣1.66(﹣2.38~﹣0.94)*** | 19.51(13.5~25.5)*** | 5.46(3.90~7.01)*** | |||||||||||||||||||||||||
模型2 | 0.02(0.01~0.03)*** | ﹣0.13(﹣0.90~0.65) | 7.80(1.3~14.3)* | 3.17(1.47~4.87)*** | |||||||||||||||||||||||||
LAD:左房内径;LVEDD:左心室舒张末期内径;LVESD:左心室收缩末期内径;IVST:舒张末期室间隔厚度;PWT:舒张末期后壁厚度;RWT:相对室壁厚度;LVEF:左心室射血分数;LVM:左心室质量;LVMI:左心室质量指数。模型1调整年龄、性别、血红蛋白、白蛋白、糖尿病、估算肾小球滤过率、血压、BMI(因LVMI已被身高2.7校正,故未再对LVMI进行校正);模型2进一步调整其他心脏标志物。sST2、NT-proBNP、hs-cTnT均为log对数转换值。*P<0.01,**P<0.001,***P<0.000 1。 |
随着肾功能减退,LVH发病率逐渐升高。LVH的发生发展与CKD患者心血管事件和死亡风险增加密切相关[3, 28]。心血管死亡风险和复合终点事件(心源性死亡、再次梗死、心力衰竭和脑卒中)风险在NG ESKD患者中最低,在CR、eLVH和cLVH患者中逐渐升高[29]。因此,预防及逆转左心室重塑及LVH是CKD患者的重要管理目标。
目前,左心室重塑的发生发展过程还不明确。大鼠模型中发现持续增加后负荷首先导致CR和cLVH,后出现左心室扩张[30]。Lind等[31]发现,随访10年后,约1/3老年cLVH患者发展为eLVH,未发现eLVH发展为cLVH案例。CREATE研究[4]也得到相似的结果。该研究对CKD 3~4期患者进行2年随访,发现1/3的cLVH患者发展为eLVH,仅8.8%~9.5%的eLVH转变为cLVH。CKD患者心脏重构及LVH的发生主要是心脏对反复容量和(或)压力过负荷的适应性重塑。其中,后负荷增加主要是高血压和血管钙化;前负荷增加包括容量过负荷和肾性贫血。后负荷增加主要诱导心室壁增厚和左室CR;前负荷增加促使心肌细胞延长、心室扩大,导致离心性重构。
NT-proBNP升高与心脏前负荷(容量过负荷)和肾脏清除率下降(如eGFR下降、晚期体液潴留)相关[32-33],而cTnT升高与心肌细胞损伤及心脏供需失衡有关。因此,这2种标志物均不能特异性提示CKD患者心脏重构。sST2是检测心脏结构变化的新型指标之一,参与心肌应激或损伤引起的心肌纤维化和炎症反应,与多种心血管疾病发生及预后相关[15-20]。在心力衰竭患者中,sST2受eGFR的影响较小[20];在CKD患者中,sST2和eGFR间中度相关,可能与CKD进展导致的心血管损伤相关[34-35]。本研究中,sST2缺乏诊断LVH的能力,但其在cLVH患者中升高明显,与既往针对高血压患者的研究[24]及在维持性HD人群中的研究[36]结果一致,而与Xanthakis等[23]的研究不同。
本研究中,sST2与心室壁增厚相关的超声参数IVST、PWT和RWT有一定正相关关系,尤其与LVMI相关,与既往研究[25]结果相似。在心衰患者中,sST2可能较NT-proBNP有更优的预后预测价值,可作为风险分层标志物[37];在一项纳入883例CKD患者的队列研究[38]中,较高水平的sST2使患者死亡率升高36%;本中心既往对HD患者的研究[39]发现,sST2可预测全因死亡率和心血管死亡率。目前临床多将sST2与其他心脏标志物联合用于病情评估,与NT-proBNP及cTnT联合可分析左心室重构情况[40]。
综上所述,在NDD-CKD患者中,sST2在伴发cLVH者中明显升高,表明IL-33/ST2通路参与心室重塑,可将sST2作为提示左心室重塑的潜在生物标志物。由于为横断面研究,本研究未能观察到心脏标志物和超声心动图参数的动态变化关系,且为单中心研究,有必要通过更大样本量研究探讨sST2在NDD-CKD患者发生LVH过程中的作用。
利益冲突: 所有作者声明不存在利益冲突。
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