软骨素的因果效应,氨基葡萄糖,和维生素/矿物质补充剂对肾功能的摄入量仍然未知,尽管常用。我们进行了两个样本的汇总水平孟德尔随机(MR)分析,以测试常规膳食补充剂摄入量与肾功能之间的因果关系。软骨素的基因仪器,氨基葡萄糖,和维生素/矿物质补充剂的摄入量来自欧洲血统的全基因组关联研究。CKDGen联盟提供了对数变换的估计肾小球滤过率(log-eGFR)的汇总统计数据。乘法随机效应逆方差加权方法表明,遗传预测的软骨素和葡糖胺摄入量与较低的eGFR(软骨素,eGFR变化β=-0.113%,标准误差(SE)=0.03%,p值=2×10-4;葡萄糖胺,eGFR变化β=-0.240%,SE=0.035%,p值=6×10-12)。然而,基因预测的维生素/矿物质补充剂摄入量与较高的eGFR相关(eGFR变化β=1.46%,SE=0.136%,p值=1×10-25)。软骨素和维生素/矿物质补充剂摄入量的验证分析和多效性稳健的MR结果支持了主要结果。我们的MR研究表明,摄入软骨素和氨基葡萄糖对肾功能具有潜在的因果关系。因此,临床医生应仔细监测其长期效果.
The causal effects of
chondroitin, glucosamine, and vitamin/mineral supplement intake on kidney function remain unknown, despite being commonly used. We conducted a two-sample summary-level Mendelian randomization (MR) analysis to test for causal associations between regular dietary supplement intake and kidney function. Genetic instruments for
chondroitin, glucosamine, and vitamin/mineral supplement intake were obtained from a genome-wide association study of European ancestry. Summary statistics for the log-transformed estimated glomerular filtration rate (log-eGFR) were provided by the CKDGen consortium. The multiplicative random-effects inverse-variance weighted method showed that genetically predicted chondroitin and glucosamine intake was causally associated with a lower eGFR (
chondroitin, eGFR change beta = -0.113%, standard error (SE) = 0.03%, p-value = 2 × 10-4; glucosamine, eGFR change beta = -0.240%, SE = 0.035%, p-value = 6 × 10-12). However, a genetically predicted vitamin/mineral supplement intake was associated with a higher eGFR (eGFR change beta = 1.426%, SE = 0.136%, p-value = 1 × 10-25). Validation analyses and pleiotropy-robust MR results for
chondroitin and vitamin/mineral supplement intake supported the main results. Our MR study suggests a potential causal effect of
chondroitin and glucosamine intake on kidney function. Therefore, clinicians should carefully monitor their long-term effects.