Department of Radiology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China.
Department of Occupational and Environmental Medicine, School of Public Health, Fudan University, Shanghai 200032, China.
Ecotoxicol Environ Saf. 2021 Mar 15;211:111933. doi: 10.1016/j.ecoenv.2021.111933. Epub 2021 Jan 25.
The association between internal cadmium exposure and chronic kidney disease (CKD) has been investigated before. However, few studies have shown the association between dietary cadmium intake and CKD. In this study, we show the association between life-time dietary cadmium intake and CKD based on a follow-up study. At baseline, we collected blood and urine samples for assays of cadmium and renal effect biomarkers. A questionnaire and food survey was given to each subject to collect diet and lifestyle information for the estimation of cadmium intake. Dietary cadmium, cadmium in blood and urine were regarded as exposure markers. Life-time dietary cadmium intake was estimated based on an individual's daily cadmium intake and exposure time. At follow-up, 467 persons (163 men and 304 women) were finally included. CKD at follow-up was considered if the estimated glomerular filtration rate (eGFR) was less than 60 mL/min/1.73 m. The eGFR level in subjects in the highest quartile of total dietary cadmium intake (>9.34 g) was significantly lower than in those with a moderate or low intake (p < 0.01). eGFR was negatively associated with total dietary cadmium intake (β = -0.42, 95% confidence interval (CI): -0.77 to -0.07) after adjustment with confounders. Logistic regression further showed that the risk of CKD in subjects with a high total dietary cadmium intake (>2.2 g) was higher than in those with a low intake (odds ratio (OR) = 18.16, 95%CI: 1.75-188.85). A similar association was found between the baseline urinary albumin (UALB) level and CKD incidence. A predictive model based on UALB and life-time dietary cadmium intake showed an acceptable performance (the area under the curve was 0.77 (95%CI: 0.65-0.88)). Our data show that high dietary cadmium exposure was associated with CKD after controlling for renal tubular dysfunction and internal cadmium exposure.
已有研究探讨了内源性镉暴露与慢性肾脏病(CKD)之间的关系。然而,很少有研究表明膳食镉摄入量与 CKD 之间存在关联。本研究基于随访研究,展示了终生膳食镉摄入量与 CKD 之间的关联。在基线时,我们采集了血液和尿液样本,用于检测镉和肾脏效应生物标志物。我们还向每位受试者发放了一份问卷和食物调查,以收集饮食和生活方式信息,从而估算镉摄入量。膳食镉、血液和尿液中的镉被视为暴露标志物。终生膳食镉摄入量基于个体的日镉摄入量和暴露时间来估算。随访时,共纳入 467 人(男性 163 人,女性 304 人)。如果估算肾小球滤过率(eGFR)<60 mL/min/1.73 m,则认为存在 CKD。总膳食镉摄入量最高四分位组(>9.34 g)受试者的 eGFR 水平明显低于中低摄入量组(p<0.01)。在校正混杂因素后,eGFR 与总膳食镉摄入量呈负相关(β=-0.42,95%置信区间(CI):-0.77 至 -0.07)。Logistic 回归进一步表明,高总膳食镉摄入量(>2.2 g)受试者发生 CKD 的风险高于低摄入量者(比值比(OR)=18.16,95%CI:1.75-188.85)。基线尿白蛋白(UALB)水平与 CKD 发生率之间也存在类似的关联。基于 UALB 和终生膳食镉摄入量的预测模型具有较好的性能(曲线下面积为 0.77(95%CI:0.65-0.88))。我们的数据表明,在控制肾小管功能障碍和内源性镉暴露后,高膳食镉暴露与 CKD 相关。