Role of CD33 basophils in mediating the effect of lipidome on chronic kidney disease: A 2-sample, 2-variable, bidirectional Mendelian randomization analysis.

This study aimed to investigate the causal relationship between lipidomes and chronic kidney disease (CKD) and identify and quantify the role of immune cells as a potential mediator. Using summary-level data from a genome-wide association study, a 2-sample Mendelian randomization (MR) analysis of genetically predicted lipidomes (7174 cases) and CKD (406,745 cases) was performed. Furthermore, we used 2-step MR to quantitate the proportion of the effect of immune cells traits-mediated lipidomes on CKD. The MR analysis revealed a causal relationship between lipidomes and CKD, with different lipidomes either increasing or decreasing the risk of CKD. Immune cells may serve as intermediaries in the pathway from lipidomes to CKD. Our study indicates that CD33 on basophils accounts for 3.23% of the reduced risk associated with triacylglycerol (53:3) levels in CKD. In conclusion, our study has identified a causal relationship between lipidomes and CKD, as well as the mediating role of CD33 on basophils. However, other risk factors like potential mediators require further investigation. In clinical practice, particular attention should be paid to lipidomic changes, especially triacylglycerol, in patients with CKD.