ArticleScientific reports2025
Complement proteins associated with circulatory and glomerular IgA-containing immune complexes in patients with IgA nephropathy.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Plasma Proteomics in IgA Nephropathy: From Circulating Biomarkers to Molecular Endotypes.Cells · 2026Review
- Inhibition of p65 NF-κB enhances production of galactose-deficient IgA1 through suppression ofbioRxiv : the preprint server for biology · 2026Article
- The biological basis of Blood-Heat syndrome in children with Henoch-Schonlein purpura nephritis: a multidimensional analysis based on clinical proteomics and an animal model.Frontiers in pharmacology · 2026Article
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Authors and funding
11 authors.
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Abstract
IgA nephropathy (IgAN) is characterized by glomerular deposits of IgA-containing immune complexes (IgA-ICs), which are suspected to originate from circulation. However, the composition of these ICs is not fully understood. To address this gap in knowledge, we performed label-free quantitative mass-spectrometry analyses of glomerular and circulatory IgA-ICs with a focus on complement proteins. Glomeruli of patients with IgAN compared to healthy glomeruli had greater amounts of several complement-system proteins associated with classical, alternative, and terminal pathways, including complement factor H-related (CFHR) proteins 1, 2, 3, and 5, C1q chains B and C, and properdin. Circulatory IgA-ICs of patients with IgAN vs. healthy controls had a greater abundance of complement proteins CFHR1, C1q chains A, B, and C, and properdin. Furthermore, levels of several complement proteins in circulatory IgA-ICs of IgAN patients were reduced after immunosuppressive therapy (i.e., tonsillectomy combined with pulse steroid therapy) but not in patients on comprehensive supportive therapy. CFHR1 exhibited the greatest decrease (Fold change = 48.16, P < 0.0001). These data together revealed the complexity of complement proteome in glomerular and circulatory IgA-ICs and suggested an association of complement regulatory proteins, such as CFHR1, with pathogenic IgA-ICs.
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