脓毒症引发急性肾损伤的生物标志物研究进展
查看参考文献33篇
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文摘
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脓毒症是由感染引起的全身炎症反应综合征(system inflammatory response syndrome,SIRS),过激的炎症反应常造成广泛的组织损伤,进一步发展为多器官功能障碍综合征(multiple organ dysfunction syndrome,MODS),甚至脓毒症休克,最终导致患者死亡,具有发病率和病死率高的特点,是临床危重症主要的死亡原因之一。急性肾损伤(acute kidney injury,AKI)是由各种原因引起的肾小球滤过率在短时间(几小时至几天)内突然和持续下降,导致含氮和非含氮代谢物蓄积而出现的临床综合征。据统计,脓毒症导致的AKI约占临床AKI疾病的50%,而当脓毒症继发AKI时,患者的病死率高达70%以上,因此AKI是最常见、最严重的脓毒症并发症之一[1]。脓毒症AKI导致患者病死率居高不下最主要的原因是临床缺乏有效、及时的诊断标准和标志物,错失最佳的治疗时机。目前,评价脓毒症病情严重程度的序贯器官功能衰竭评分(sequential organ failure assessment,SOFA)、AKI临床诊断常用的风险期、损伤期、衰竭期、丧失期和终末期肾病(risk,injury,failure,loss,end stage kidney disease,RIFLE)及急性肾损伤网络(acute kidney injury network,AKIN)分级诊断标准均以血清肌酐的升高程度及尿量的减少水平为参考。然而,自身代谢水平的差异、临床药物的使用及液体复苏治疗等均会影响脓毒症患者的血清肌酐水平,并且血清肌酐升高要比肾脏出现损伤延迟2~ 3 d;尿量则更容易受到患者利尿剂的使用以及尿路堵塞等问题的干扰,因此,血清肌酐及尿量并不能作为脓毒症AKI早期诊断的可靠标志物[2]。通过微透析等先进在体取样技术,寻求更加敏感、特异性强的脓毒症AKI生物标志物是目前亟待解决的难题之一。近年来,医学界为寻求更加敏感的脓毒症AKI早期生物标志物做了大量研究,本文对具有代表性的生物标志物进行系统的梳理分析,为临床选择更加适宜的诊断指标提供信息支持,最终为尽快实现脓毒症AKI的早期临床诊断与治疗打下基础。 |
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来源
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中华危重症医学杂志(电子版)
,2017,10(1):53-57 【扩展库】
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DOI
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10.3877/cma.j.issn.1674-6880.2017.01.013
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关键词
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脓毒症
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急性肾损伤
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生物标志物
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地址
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1.
火箭军总医院药学部, 北京, 100088
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火箭军总医院骨科, 北京, 100088
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语种
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中文 |
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文献类型
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综述型 |
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ISSN
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1674-6880 |
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学科
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临床医学;外科学 |
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基金
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国家自然科学基金青年科学基金项目
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火箭军总医院青年科研创新基金项目
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北京市科技新星与领军人才培养专项
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文献收藏号
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CSCD:5972977
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