AI Article Synopsis

  • The study investigates the role of urinary proteins and hypercoagulability in the development of IgA vasculitis (IgAV) by comparing the urinary biomarkers of healthy children and those with IgAV.
  • Using advanced techniques, researchers identified 772 proteins with significant differences, with key findings highlighting the involvement of proteins like thrombin and macrophage migration inhibitory factor (MIF) in inflammatory and coagulation pathways.
  • Results suggest that increased levels of urinary thrombin and MIF can serve as effective biomarkers for assessing inflammatory and hypercoagulable states in children suffering from IgAV.

Article Abstract

Objectives: To explore the evidence, urinary biomarkers, and partial mechanisms of hypercoagulability in the pathogenesis of IgA vasculitis (IgAV).

Methods: Differential expression of proteins in the urine of 10 healthy children and 10 children with IgAV was screened using high-performance liquid chromatography-tandem mass spectrometry, followed by Reactome pathway analysis. Protein-protein interaction (PPI) network analysis was conducted using STRING and Cytoscape software. In the validation cohort, 15 healthy children and 25 children with IgAV were included, and the expression levels of differential urinary proteins were verified using enzyme-linked immunosorbent assay.

Results: A total of 772 differential proteins were identified between the IgAV group and the control group, with 768 upregulated and 4 downregulated. Reactome pathway enrichment results showed that neutrophil degranulation, platelet activation, and hemostasis pathways were involved in the pathogenesis of IgAV. Among the differential proteins, macrophage migration inhibitory factor (MIF) played a significant role in neutrophil degranulation and hemostasis, while thrombin was a key protein in platelet activation and hemostasis pathways. PPI analysis indicated that thrombin directly interacted with several proteins involved in inflammatory responses, and these interactions involved MIF. Validation results showed that compared to healthy children, children with IgAV had significantly higher urine thrombin/creatinine and urine MIF/creatinine levels (<0.05).

Conclusions: Thrombin contributes to the pathogenesis of IgAV through interactions with inflammatory factors. Urinary thrombin and MIF can serve as biomarkers reflecting the hypercoagulable and inflammatory states in children with IgAV.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11562050PMC
http://dx.doi.org/10.7499/j.issn.1008-8830.2311151DOI Listing

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