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急性肾损伤生物标志物的漫漫求索之路。

A long journey for acute kidney injury biomarkers.

机构信息

Division of Nephrology, Department of Internal Medicine, Myongji Hospital, Hanyang University College of Medicine, Goyang, Korea.

出版信息

Ren Fail. 2020 Nov;42(1):154-165. doi: 10.1080/0886022X.2020.1721300.

DOI:10.1080/0886022X.2020.1721300
PMID:32050834
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7034110/
Abstract

Acute kidney injury (AKI) is a life-threatening illness that continues to have an in-hospital mortality rate of patients with AKI ranges from 20% to 50% or greater, depending on underlying conditions. However, it has only marginally declined over the past 25 years. Previous authoritative publications have been pointed out that the lack of useful biomarkers for AKI has limited progress in improving the outcomes of this disorder. The purpose of this paper is to review the recent biomarkers involved in the early detection of AKI and main reasons for the failure to identify new AKI biomarkers. So far, several new AKI biomarkers have been discovered and validated to improve early diagnosis, degree of severity, pathophysiology, differential diagnosis, prediction for major kidney adverse events (MAKE, risk groups for progressive renal failure, need for renal replacement therapy [RRT], or death). These biomarkers can be classified into functional, damage and pre-injury phase biomarkers. However, the clinical use of the studied biomarkers in AKI prediction remains unclear because large prospective multicenter trials have failed to demonstrate troponin-like diagnostic performance. Reasons for the failure to identify AKI biomarkers are the heterogeneity of AKI itself, biomarker limitations and long roads to the validation of candidates for new AKI biomarkers. In an effort to overcome these barriers to identifying new AKI biomarkers, kidney biopsy specimens should be obtained and assessed in human AKI populations. Research in this field should be carried out in a pan-social approach rather than conducted by just a few medical institutions.

摘要

急性肾损伤(AKI)是一种危及生命的疾病,患有 AKI 的患者的院内死亡率范围为 20%至 50%或更高,具体取决于基础疾病。然而,在过去的 25 年中,这一数字仅略有下降。先前的权威出版物指出,缺乏有用的 AKI 生物标志物限制了改善这种疾病结局的进展。本文的目的是回顾最近涉及 AKI 早期检测的生物标志物,以及未能确定新的 AKI 生物标志物的主要原因。到目前为止,已经发现并验证了几种新的 AKI 生物标志物,以改善早期诊断、严重程度、病理生理学、鉴别诊断、对主要肾脏不良事件(MAKE、肾功能衰竭进展风险组、需要肾脏替代治疗[RRT]或死亡)的预测。这些生物标志物可以分为功能、损伤和损伤前阶段的生物标志物。然而,研究生物标志物在 AKI 预测中的临床应用仍不明确,因为大型前瞻性多中心试验未能证明肌钙蛋白样诊断性能。未能确定 AKI 生物标志物的原因是 AKI 本身的异质性、生物标志物的局限性以及新的 AKI 生物标志物候选物的验证道路漫长。为了克服确定新的 AKI 生物标志物的这些障碍,应在人类 AKI 人群中获取和评估肾活检标本。应该以泛社会的方法进行该领域的研究,而不仅仅是由少数医疗机构进行。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad74/7034110/447c6a51c964/IRNF_A_1721300_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad74/7034110/d59c864ec9ce/IRNF_A_1721300_F0001_B.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad74/7034110/447c6a51c964/IRNF_A_1721300_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad74/7034110/d59c864ec9ce/IRNF_A_1721300_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad74/7034110/35c21790c94f/IRNF_A_1721300_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad74/7034110/eb638ff537d3/IRNF_A_1721300_F0003_C.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad74/7034110/447c6a51c964/IRNF_A_1721300_F0005_C.jpg

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