ArticleEuropean journal of immunology2018
Complement factor H protects mice from ischemic acute kidney injury but is not critical for controlling complement activation by glomerular IgM.
Article in European journal of immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Rationale for Targeting Complement to Mitigate Renal Transplant Ischemia-Reperfusion Injury.Journal of the American Society of Nephrology : JASN · 2026Review
- Redox Regulation of Complement Pathway Activation in Aging and Related Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Exploring Potential Complement Modulation Strategies for Ischemia-Reperfusion Injury in Kidney Transplantation.Antioxidants (Basel, Switzerland) · 2025Review
- The complement system in pediatric acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2023Review
- The Complement System in Kidney Transplantation.Cells · 2023Review
- Factor H related proteins modulate complement activation on kidney cells.Kidney international · 2022Article
- Role of Complement System in Kidney Transplantation: Stepping From Animal Models to Clinical Application.Frontiers in immunology · 2022Review
- Activation of final complement components after kidney transplantation as a marker of delayed graft function severity.Clinical kidney journal · 2021Article
- Role of C5aR1 and C5L2 Receptors in Ischemia-Reperfusion Injury.Journal of clinical medicine · 2021Article
- Circulating FH Protects Kidneys From Tubular Injury During Systemic Hemolysis.Frontiers in immunology · 2020Article
- Urine complement activation fragments are increased in patients with kidney injury after cardiac surgery.American journal of physiology. Renal physiology · 2019Article
- The role of complement in antibody mediated transplant rejection.Molecular immunology · 2019Review
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
Natural IgM binds to glomerular epitopes in several progressive kidney diseases. Previous work has shown that IgM also binds within the glomerulus after ischemia/reperfusion (I/R) but does not fully activate the complement system. Factor H is a circulating complement regulatory protein, and congenital or acquired deficiency of factor H is a strong risk factor for several types of kidney disease. We hypothesized that factor H controls complement activation by IgM in the kidney after I/R, and that heterozygous factor H deficiency would permit IgM-mediated complement activation and injury at this location. We found that mice with targeted heterozygous deletion of the gene for factor H developed more severe kidney injury after I/R than wild-type controls, as expected, but that complement activation within the glomeruli remained well controlled. Furthermore, mice that are unable to generate soluble IgM were not protected from renal I/R, even in the setting of heterozygous factor H deficiency. These results demonstrate that factor H is important for limiting injury in the kidney after I/R, but it is not critical for controlling complement activation by immunoglobulin within the glomerulus in this setting. IgM binds to glomerular epitopes after I/R, but it is not a significant source of injury.
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