目的：探究血清尿酸（SUA）水平是否与脑小血管病（CSVD）存在因果关系。方法：从已发表的全基 因组关联研究汇总数据获得SUA、腔隙性脑梗死（LI）、白质高信号（WMH）、各向异性分数（FA）和平均弥 散率（MD）的数据，筛选出与 SUA 强相关（F＞10）的单核苷酸多态性（SNPs）作为工具变量，用逆方差加 权法、MR-Egger、加权中位数法方法进行因果分析，利用MR-Egger截距法和Cochran's Q检验进行异质性 和水平多效性检验。结果：逆方差加权法表明SUA与LI（OR=1.086，95%CI 0.959～1.230，P=0.193）、WMH （OR=1.010，95% CI 0.956～1.066，P=0.725）、FA（OR=1.058，95% CI 0.848～1.320，P=0.617）和 MD（OR= 1.009，95%CI 0.790～1.288，P=0.943）无关，敏感性分析结果显示无异质性和水平多效性。结论：目前MR研 究表明SUA水平与CSVD之间不存在因果关系，但仍需规范化、大样本的临床研究和基于大规模GWAS的 MR研究更全面评估它们之间的关联性。

To explore whether there is a causal relation between serum uric acid (SUA) levels and cerebral small vessel disease(CSVD). Methods: Data of SUA, lacunar infarction (LI), white matter hyperintensitie (WMH), fractional anisotropy (FA) and mean diffusivity (MD) were obtained from published genome-wide association study. Single nucleotide polymorphisms (SNPs) strongly associated with SUA (F-statistic>10) were selected as instrumental variables, and causal analysis is carried out by inverse variance weighted, MR-Egger, and Weighted median method. Meanwhile, the heterogeneity and horizontal pleiotropic tests were performed using MR-Egger intercept test and Cochran's Q test. Results: Inverse variance weighted showed that SUA was not associated with LI (OR=1.086, 95%CI 0.959～1.230, P=0.193), WMH (OR=1.010, 95%CI 0.956～1.066, P=0.725), FA (OR=1.058, 95%CI 0.848～1.320, P=0.617) and MD (OR=1.009, 95%CI 0.790～1.288, P=0.943). Moreover, sensitivity analysis showed no heterogeneity and horizontal pleiotropy. Conclusion: Current MR Studies had shown no causal relationship between SUA and CSVD, but standardized, large-sample clinical studies and large-scale GWAS-based MR Studies are needed to more fully evaluate the association.