预防急性肾损伤的促红细胞生成剂。

IF 8.8 2区 医学 Q1 MEDICINE, GENERAL & INTERNAL Cochrane Database of Systematic Reviews Pub Date : 2024-09-20 DOI:10.1002/14651858.CD014820.pub2
Hiroki Nishiwaki, Yoshifusa Abe, Taihei Suzuki, Takeshi Hasegawa, William Mm Levack, Hisashi Noma, Erika Ota
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引用次数: 0

摘要

背景:急性肾损伤(AKI)的特点是肾功能急剧下降,由多种临床症状引起。急性肾损伤在住院成人中的发病率很高。在动物实验中,红细胞生成刺激剂(ESA)通过抑制细胞凋亡、促进细胞增殖、诱导抗氧化和抗炎反应,对缺血性、中毒性和化脓性 AKI 起着新型肾保护作用。因此,ESAs 可降低人类 AKI 的发病率。目前已就 ESA 的疗效和安全性进行了随机对照试验 (RCT),但还没有系统性综述对 ESA 预防 AKI 进行全面研究,尽管这些药物对一系列其他疾病和临床情况的疗效进行了研究:本综述旨在研究ESAs在任何健康状况下预防AKI的益处和危害:我们通过与信息专家联系,使用与本综述相关的检索词检索了截至 2024 年 8 月 30 日的 Cochrane 肾脏与移植研究登记册。登记册中的研究是通过检索 CENTRAL、MEDLINE 和 EMBASE、会议论文集、国际临床试验登记平台 (ICTRP) 搜索门户和 ClinicalTrials.gov 确定的:我们纳入了在有 AKI 风险的人群中比较 ESA 与安慰剂或标准护理的 RCT 和准 RCT(其中治疗分配基于交替分配或病历顺序、入院日期、出生日期或其他非随机方法):三位作者独立提取数据并评估纳入研究的偏倚风险。我们使用随机效应模型荟萃分析对数据进行定量综合。我们使用 I2 统计量来衡量每项分析中研究之间的异质性。对于二分结果,我们用风险比 (RR) 表示简要估计值;对于连续结果,我们用平均差 (MD) 表示简要估计值,并附有 95% 的置信区间 (CI)。我们采用推荐、评估、发展和评价分级法(GRADE)对每个主要结果的证据确定性进行了评估:共纳入 20 项研究(36 条记录,5348 名参与者)。参与者人数从 10 人到 1302 人不等,大多数研究在单个中心进行(13/20)。所有纳入的研究都将ESAs与安慰剂或常规护理进行了比较。许多研究被认为存在不明确或高风险的报告偏倚,但其他类型的偏倚风险较低。与对照干预相比,ESAs 对 AKI 风险的影响很小或没有影响(18 项研究,5314 名参与者:RR 0.97, 95% CI 0.85 to 1.10; I² = 19%; 中度确定性证据)、死亡(18 项研究,5263 名参与者:RR 0.92,95% CI 0.80 至 1.06;I² = 0%;中度确定性证据),或开始透析(14 项研究,2059 名参与者:RR 1.16,95% CI 0.90 至 1.51;I² = 0%;低度确定性证据)。即使对 AKI 进行了标准化测量,研究结果显示,不同给药途径(皮下注射或静脉注射)、背景疾病(心脏手术、儿童或新生儿、有 AKI 风险的其他成人)、ESA 持续时间或剂量之间的结果也没有差异。与对照干预相比,ESAs对血栓形成风险的影响可能很小或没有影响(8 项研究,3484 名参与者:RR 0.92,95% CI 0.68 至 1.24;I² = 0%)。同样,肾功能指标和不良事件(如心肌梗死、中风或高血压)可能也没有差异。然而,这可能是由于这些不良事件的发生率较低:作者的结论:对于有发生 AKI 风险的患者,ESAs 可能不会降低发生 AKI 或死亡的风险,也可能不会减少开始透析的需要。同样,肾功能指标和血栓形成、心肌梗塞、中风或高血压等不良事件也可能没有差异。目前有两项正在进行的研究尚未完成或发表,尚不清楚它们是否会改变研究结果。使用ESAs预防AKI时应谨慎。
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Erythropoiesis-stimulating agents for preventing acute kidney injury.

Background: Acute kidney injury (AKI) is characterised by a rapid decline in kidney function and is caused by a variety of clinical conditions. The incidence of AKI in hospitalised adults is high. In animal studies, erythropoiesis-stimulating agents (ESA) have been shown to act as a novel nephroprotective agent against ischaemic, toxic, and septic AKI by inhibiting apoptosis, promoting cell proliferation, and inducing antioxidant and anti-inflammatory responses. As a result, ESAs may reduce the incidence of AKI in humans. Randomised controlled trials (RCTs) have been conducted on the efficacy and safety of ESAs, but no prior systematic reviews exist that comprehensively examine ESAs with respect to AKI prevention, although the effectiveness of these agents has been examined for a range of other diseases and clinical situations.

Objectives: This review aimed to look at the benefits and harms of ESAs for preventing AKI in the context of any health condition.

Search methods: We searched the Cochrane Kidney and Transplant Register of Studies up to 30 August 2024 through contact with the Information Specialist using search terms relevant to this review. Studies in the Register are identified through searches of CENTRAL, MEDLINE, and EMBASE, conference proceedings, the International Clinical Trials Registry Platform (ICTRP) Search Portal and ClinicalTrials.gov.

Selection criteria: We included RCTs and quasi-RCTs (in which allocation to treatment was based on alternate assignment or order of medical records, admission dates, date of birth or other non-random methods) that compared ESAs with placebo or standard care in people at risk of AKI.

Data collection and analysis: Three authors independently extracted data and assessed the risk of bias for included studies. We used random-effects model meta-analyses to perform quantitative synthesis of the data. We used the I2 statistic to measure heterogeneity amongst the studies in each analysis. We indicated summary estimates as a risk ratio (RR) for dichotomous outcomes and mean difference (MD) for continuous outcomes with their 95% confidence interval (CI). We assessed the certainty of the evidence for each main outcome using the Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) approach.

Main results: A total of 20 studies (36 records, 5348 participants) were included. The number of participants ranged from 10 to 1302, and most studies were carried out in single centres (13/20). All the included studies compared ESAs to placebo or usual care. Many of the studies were judged to have unclear or high risk of reporting bias, but were at low risk for other types of bias. ESAs, when compared to control interventions, probably makes little or no difference to the risk of AKI (18 studies, 5314 participants: RR 0.97, 95% CI 0.85 to 1.10; I² = 19%; moderate-certainty evidence), or death (18 studies, 5263 participants: RR 0.92, 95% CI 0.80 to 1.06; I² = 0%; moderate-certainty evidence), and may make little or no difference to the initiation of dialysis (14 studies, 2059 participants: RR 1.16, 95% CI 0.90 to 1.51; I² = 0%; low-certainty evidence). Even with standardised measurement of AKI, the studies showed no difference in results between different routes of administration (subcutaneous or intravenous), background diseases (cardiac surgeries, children or neonates, other adults at risk of AKI), or duration or dose of ESA. ESAs may make little or no difference to the risk of thrombosis when compared to control interventions (8 studies, 3484 participants: RR 0.92, 95% CI 0.68 to 1.24; I² = 0%). Similarly, ESAs may have little or no effect on kidney function measures and adverse events such as myocardial infarction, stroke or hypertension. However, this may be due to the low incidence of these adverse events.

Authors' conclusions: In patients at risk of AKI, ESAs probably do not reduce the risk of AKI or death and may not reduce the need for starting dialysis. Similarly, there may be no differences in kidney function measures and adverse events such as thrombosis, myocardial infarction, stroke or hypertension. There are currently two ongoing studies that have either not been completed or published, and it is unclear whether they will change the results. Caution should be exercised when using ESAs to prevent AKI.

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来源期刊
CiteScore
10.60
自引率
2.40%
发文量
173
审稿时长
1-2 weeks
期刊介绍: The Cochrane Database of Systematic Reviews (CDSR) stands as the premier database for systematic reviews in healthcare. It comprises Cochrane Reviews, along with protocols for these reviews, editorials, and supplements. Owned and operated by Cochrane, a worldwide independent network of healthcare stakeholders, the CDSR (ISSN 1469-493X) encompasses a broad spectrum of health-related topics, including health services.
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