Association between cadmium exposure and risk of chronic kidney disease; a systematic review and meta-analysis

IF 0.2 Q4 UROLOGY & NEPHROLOGY
Mehrdad Abbaszadeh, Hassan Pakdel, Somayeh Barakeh, Ahmad Pakdel
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引用次数: 0

Abstract

Introduction: Chronic kidney disease (CKD) is the twelfth most common cause of death worldwide. The kidneys are the primary site of cadmium accumulation and the most sensitive organ to cadmium toxicity. Therefore, the current study aimed to investigate the relationship between cadmium exposure and the risk of CKD using a systematic review and meta-analysis method. Materials and Methods: In this systematic review and meta-analysis, databases including PubMed, Scopus, Web of Science, Cochrane, and Google Scholar were searched without time restrictions until September 9, 2023. Data were analyzed using STATA 14 software, and P <0.05 was considered statistically significant. Results: The results of combining 18 observational studies with a total of 230,790 participants showed that an increase in blood cadmium levels was associated with an increased risk of CKD (OR: 1.42; 95% CI: 1.18, 1.70). This association was significant in cross-sectional studies (OR: 1.21; 95% CI: 1.04, 1.41), case-control studies (OR: 3.08; 95% CI: 1.47, 6.41), and cohort studies (OR: 1.36; 95% CI: 0.85, 2.17). Generally, the relationship between urinary cadmium levels and CKD was not statistically significant (OR: 1.14; 95% CI: 0.84, 1.54). In cross-sectional studies, high urinary cadmium levels reduced the risk of CKD (OR: 0.77; 95% CI: 0.60, 0.99). However, in case-control studies, the relationship between high urinary cadmium levels and risk of CKD was not statistically significant (OR: 0.20; 95% CI: 0.02, 2.40). Since in cohort studies, high urinary cadmium levels were a risk factor for CKD (OR: 1.40; 95% CI: 1.07, 1.83)]. The relationship between cadmium consumption and the risk of CKD was statistically significant (OR: 1.55; 95% CI: 1.00, 2.42), with significance in case-control studies (OR: 18.16; 95% CI: 1.75, 188.64) but not in cohort studies (OR: 1.45; 95% CI: 0.93, 2.25). Conclusion: Overall, an increase in blood cadmium levels was associated with a 42% increased risk of CKD. Furthermore, cadmium consumption through the diet increased the risk of CKD by 55%. Registration: This study has been compiled based on the PRISMA checklist, and its protocol was registered on the PROSPERO (ID: CRD42023463145).
镉暴露与慢性肾病风险之间的关系;系统回顾和荟萃分析
简介慢性肾脏病(CKD)是全球第十二大常见死因。肾脏是镉积累的主要部位,也是对镉毒性最敏感的器官。因此,本研究旨在采用系统回顾和荟萃分析方法,探讨镉暴露与慢性肾脏病风险之间的关系。材料与方法:在本系统综述和荟萃分析中,对包括 PubMed、Scopus、Web of Science、Cochrane 和 Google Scholar 在内的数据库进行了无时间限制的检索,直至 2023 年 9 月 9 日。数据使用 STATA 14 软件进行分析,P <0.05 为具有统计学意义。结果综合 18 项观察性研究(共 230,790 人参与)的结果显示,血液中镉含量的增加与慢性肾脏病风险的增加有关(OR:1.42;95% CI:1.18, 1.70)。这种关联在横断面研究(OR:1.21;95% CI:1.04,1.41)、病例对照研究(OR:3.08;95% CI:1.47,6.41)和队列研究(OR:1.36;95% CI:0.85,2.17)中都很明显。一般来说,尿镉水平与慢性肾脏病之间的关系并无统计学意义(OR:1.14;95% CI:0.84,1.54)。在横断面研究中,尿镉水平高会降低患慢性肾脏病的风险(OR:0.77;95% CI:0.60,0.99)。然而,在病例对照研究中,尿镉含量高与患慢性肾脏病风险之间的关系在统计学上并不显著(OR:0.20;95% CI:0.02,2.40)。而在队列研究中,高尿镉水平是导致慢性肾脏病的风险因素(OR:1.40;95% CI:1.07,1.83)]。镉摄入量与患慢性肾脏病风险之间的关系具有统计学意义(OR:1.55;95% CI:1.00,2.42),在病例对照研究中具有显著性(OR:18.16;95% CI:1.75,188.64),但在队列研究中不具有显著性(OR:1.45;95% CI:0.93,2.25)。结论总体而言,血液中镉含量的增加与患慢性肾脏病的风险增加 42% 有关。此外,通过饮食摄入镉会使患慢性肾脏病的风险增加 55%。注册:本研究根据PRISMA核对表编制,其研究方案已在PROSPERO(ID:CRD42023463145)上注册。
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来源期刊
Journal of Renal Injury Prevention
Journal of Renal Injury Prevention UROLOGY & NEPHROLOGY-
CiteScore
1.60
自引率
0.00%
发文量
36
期刊介绍: The Journal of Renal Injury Prevention (JRIP) is a quarterly peer-reviewed international journal devoted to the promotion of early diagnosis and prevention of renal diseases. It publishes in March, June, September and December of each year. It has pursued this aim through publishing editorials, original research articles, reviews, mini-reviews, commentaries, letters to the editor, hypothesis, case reports, epidemiology and prevention, news and views and renal biopsy teaching point. In this journal, particular emphasis is given to research, both experimental and clinical, aimed at protection/prevention of renal failure and modalities in the treatment of diabetic nephropathy. A further aim of this journal is to emphasize and strengthen the link between renal pathologists/nephropathologists and nephrologists. In addition, JRIP welcomes basic biomedical as well as pharmaceutical scientific research applied to clinical nephrology. Futuristic conceptual hypothesis that integrate various fields of acute kidney injury and renal tubular cell protection are encouraged to be submitted.
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