Objective: The aim was to study the preliminary screening of the crucial genes in intimal hyperplasia in the venous segment of arteriovenous (AV) fistula and the underlying potential molecular mechanisms of intimal hyperplasia with bioinformatics analysis.Methods: The gene expression profile data (GSE39488) was analyzed to identify differentially expressed genes (DEGs). We performed Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of DEGs. Gene set enrichment analysis (GSEA) was used to understand the potential activated signaling pathway. The protein–protein interaction (PPI) network was constructed with the STRING database and Cytoscape software. The Venn diagram between 10 hub genes and gene sets of 4 crucial signaling pathways was used to obtain core genes and relevant potential pathways. Furthermore, GSEAs were performed to understand their biological functions.Results: A total of 185 DEGs were screened in this study. The main biological function of the 111 upregulated genes in AV fistula primarily concentrated on cell proliferation and vascular remodeling, and the 74 downregulated genes in AV fistula were enriched in the biological function mainly relevant to inflammation. GSEA found four signaling pathways crucial for intimal hyperplasia, namely, MAPK, NOD-like, Cell Cycle, and TGF-beta signaling pathway. A total of 10 hub genes were identified, namely, EGR1, EGR2, EGR3, NR4A1, NR4A2, DUSP1, CXCR4, ATF3, CCL4, and CYR61. Particularly, DUSP1 and NR4A1 were identified as core genes that potentially participate in the MAPK signaling pathway. In AV fistula, the biological processes and pathways were primarily involved with MAPK signaling pathway and MAPK-mediated pathway with the high expression of DUSP1 and were highly relevant to cell proliferation and inflammation with the low expression of DUSP1. Besides, the biological processes and pathways in AV fistula with the high expression of NR4A1 similarly included the MAPK signaling pathway and the pathway mediated by MAPK signaling, and it was mainly involved with inflammation in AV fistula with the low expression of NR4A1.Conclusion: We screened four potential signaling pathways relevant to intimal hyperplasia and identified 10 hub genes, including two core genes (i.e., DUSP1 and NR4A1). Two core genes potentially participate in the MAPK signaling pathway and might serve as the therapeutic targets of intimal hyperplasia to prevent stenosis after AV fistula creation.

Objective: To compare central venous stenosis/occlusion with or without previous jugular catheter placement history.Methods: Data of patients with central vein stenosis/occlusion receiving endovascular intervention in our hospital from January 2015 to December 2018 were collected and analyzed.Results: Twenty-nine patients with previous jugular catheter placement history (CVC group) and 33 patients (excluded two with technical failure) without such history (non-CVC group) are included in this study. Previous jugular catheter placement history raised the risk of postintervention recurrence 1.02 times (CVC group vs. non-CVC group, HR = 2.02 95%CI: 0.91–4.48). The primary patency rate at 6, 12, 18, and 24 months was 76.9, 54.2, 45.5, and 25.0% separately in the CVC group and 80.6, 70.0, 67.9, and 44.4% separately in the non-CVC group. The assisted primary patency rate at 6, 12, 18, and 24 months was 92.3, 91.7, 86.4, and 68.8% separately in the CVC group and 93.5, 90.0, 82.1, and 61.1% separately in the non-CVC group. Patients in the CVC group received a higher frequency of reintervention (0.7 times/year/patient vs. 0.3 times/year/patient). There was no significant difference in the assisted primary patency rate between the two groups. Different primary interventions (angioplasty alone, bare metal stent, stent graft) did not affect primary patency and assisted primary patency, but percutaneous transluminal stenting (PTS) with a bare metal stent had a significant lower primary patency rate between 3 and 24 months compared with PTS with a stent graft (p = 0.011).Conclusion: Central venous stenosis/occlusion with a previous jugular catheter placement history develops symptoms earlier and had a worse prognosis after endovascular intervention. More efforts are needed to carry out end-stage kidney disease life plan to reduce the harm of evitable catheter placement.

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