Objective @#To explore the candidate genes and potential molecular mechanisms of anti -neutrophil cyto- plasmic antibodies ( ANCA) -associated vasculitis by bioinformatics and experimental validation , and to provide a scientific theoretical basis for the treatment of potential inflammatory targets for ANCA-associated vasculitis .@*Methods@#The GSE108109 chip data was retrieved from the Gene Expression Omnibus (GEO) database , and the differential genes were processed , analyzed and screened using the R language related program package . Kyoto encyclo- pedia of genes and genomes (KEGG) and gene ontology (GO) enrichment analysis was carried out using DAVID online network cable , and the interaction network of the protein encoded by the selected genes of inflammatory syn- drome was constructed through STRING web site . Further endogenous competitive RNA ( ceRNA) regulatory net- work was predicted and constructed through miRWalk and DIANA-LncBase databases , and key genes were screened from the network to draw ROC curve . The renal biopsy samples of patients with ANCA-associated vasculi- tis confirmed by our hospital were collected as the experimental group , and the renal biopsy samples of IgA ne- phropathy and micro-adaptive nephropathy were collected as the control group . Immunohistochemical staining was performed on the collected renal biopsy samples , and the average optical density was calculated by semi -quantita- tive analysis of immunohistochemical staining to further verify the expression of the key genes screened by the bioin- formatics analysis . Pearson linear correlation analysis was performed between the average optical density results and the clinical inflammatory data of patients . @*Results @#846 differential genes were screened , of which 444 genes were significantly up-regulated and 402 genes were significantly down-regulated . Through KEGG and GO analysis , im- portant differentially expressed genes related to inflammation regulation were obtained . Among them , CSF1R and TNFRSF1B , two differentially expressed genes never reported in ANCA-associated vasculitis , attracted our atten- tion . At the same time , we constructed multiple ceRNA regulatory axes including KCNQ1OT1 -hsa-miR-125 a-5p- TNFRSF1B . There were 15 samples of ANCA-associated vasculitis , 6 samples of IgA nephropathy , and 3 samples of micropathological kidney . Immunohistochemical results of renal biopsy specimens showed that the expression of CSF1R and TNFRSF1B in ANCA-associated vasculitis kidney tissue was higher than that in the control group . Pearson correlation analysis of clinical data of patients in ANCA group showed that the expression of CSF1R was positively correlated with the content of neutrophil count ( r = 0. 587) , and the expression of TNFRSF1B was posi- tively correlated with the content of serum C -reactive protein ( r = 0. 646) . @*Conclusion @#Key genes related to in- flammatory regulation such as CSF1R and TNFRSF1B were investigated by bioinformatics methods , and a rigorous ceRNA regulatory network was constructed . The expression of CSF1R and TNFRSF1B in ANCA vasculitis was high- er than that in the control group through immunohistochemistry . The results provides a scientific theoretical basis for the molecular mechanism of inflammation , and laid a good foundation for new therapeutic targets of ANCA-related vasculitis for inflammation .