ArticleJournal of the American Society of Nephrology : JASN2013
IgM contributes to glomerular injury in FSGS.
Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 105 citations in OpenAlex.
- Complement role in kidney disease: a comprehensive review and therapeutic innovations.BMC nephrology · 2026Review
- Combined Anti-CD20/Anti-CD38 Therapy in Posttransplant Focal Segmental Glomerulosclerosis Recurrence: A Retrospective, International, Multicenter Study.Transplantation direct · 2026Article
- Multi-omics analyses demonstrate complement dysregulation is involved in focal segmental glomerulosclerosis.Frontiers in immunology · 2026Article
- Significant glomerular IgM deposition predicts poorer kidney outcomes in lupus nephritis compared with other forms of immune complex deposits.Lupus science & medicine · 2025Article
- Comprehensive analysis of the clinical and pathological features and prognoses of children with immunoglobulin A vasculitis nephritis with immunoglobulin M deposits in glomeruli.Kidney research and clinical practice · 2025Article
- Article
- Clinical Significance of Immune Deposits and Complement System Activation in FSGS: Findings from the Cure Glomerulonephropathy Network Study.Kidney360 · 2025Article
- To biopsy or not to biopsy a teenager with idiopathic nephrotic syndrome? Biopsy first.Pediatric nephrology (Berlin, Germany) · 2025Article
- The role of B lymphocyte subsets in nephrotic syndrome: functions, mechanisms, clinical significance and future perspectives.Frontiers in immunology · 2025Review
- Clinical significance of concomitant IgM and C3 deposition in patients with focal segmental glomerulosclerosis.Journal of nephrology · 2025Article
- Immunoglobulin M nephropathy: requiring more attention.Kidney research and clinical practice · 2025Article
- Prognostic role of mesangial IgM deposition in IgA nephropathy: a long-term cohort study.Renal failure · 2024Article
- Apical tubular complement activation and the loss of kidney function in proteinuric kidney diseases.Clinical kidney journal · 2024Review
- The Lectin Pathway-A Dominant Pattern of the Complement System Activation in Primary Focal Segmental Glomerulosclerosis?Kidney international reports · 2024Article
- Management of adult patients with podocytopathies: an update from the ERA Immunonephrology Working Group.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024Article
- The fate of immune complexes in membranous nephropathy.Frontiers in immunology · 2024Review
- The role of complement in kidney disease.Nature reviews. Nephrology · 2023Review
- Clinical significance of IgM and C3 deposition in children with primary immunoglobulin A nephropathy.Journal of nephrology · 2023Article
- Female but Not Male Mice Deficient in Soluble IgM Are Susceptible to Chemically Induced Glomerular Injury.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- A clinicopathological and prognostic study of 18 children with C1q nephropathy and focal segmental glomerulosclerosis: an 18-year experience from a single center.Journal of nephrology · 2023Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Glomerular IgM and C3 deposits frequently accompany idiopathic FSGS and secondary glomerulosclerosis, but it is unknown whether IgM activates complement, possibly contributing to the pathogenesis of these diseases. We hypothesized that IgM natural antibody binds to neoepitopes exposed in the glomerulus after nonimmune insults, triggering activation of the complement system and further injury. We examined the effects of depleting B cells, using three different strategies, on adriamycin-induced glomerulosclerosis. First, we treated wild-type mice with an anti-murine CD20 antibody, which depletes B cells, before disease induction. Second, we evaluated adriamycin-induced glomerulosclerosis in Jh mice, a strain that lacks mature B cells. Third, we locally depleted peritoneal B cells via hypotonic shock before disease induction. All three strategies reduced deposition of IgM in the glomerulus after administration of adriamycin and attenuated the development of albuminuria. Furthermore, we found that glomerular IgM and C3 were detectable in a subset of patients with FSGS; C3 was present as an activation fragment and colocalized with glomerular IgM, suggesting that glomerular IgM may have bound a cognate ligand. Taken together, these results suggest that IgM activates the complement system within the glomerulus in an animal model of glomerulosclerosis. Strategies that reduce IgM natural antibody or that prevent complement activation may slow the progression of glomerulosclerosis.
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