ArticleJournal of the American Society of Nephrology : JASN2011
Complement factor H deficiency accelerates development of lupus nephritis.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 126 citations in OpenAlex.
- Multimodal Profiling of Complement Expression and Association With Outcomes in ANCA-Associated Vasculitis With Glomerulonephritis.Kidney international reports · 2026Article
- Complement and kidney diseases: unlocking the opportunity of targeted treatments for glomerular diseases, including IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2026Review
- Immunopathogenesis of Systemic Lupus Erythematosus: Interplay of Innate and Adaptive Immunity, Microbiome Dysbiosis, and Emerging Therapeutic Targets.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- Isolated C3 hypocomplementemia as an early predictor of chronic kidney disease in lupus nephritis.Frontiers in immunology · 2025Observational
- Article
- Animal models of lupus nephritis: the past, present and a future outlook.Autoimmunity · 2024Review
- Systemic lupus erythematosus presenting with atypical hemolytic uremic syndrome: a case report and review of the literature.Rheumatology international · 2024Review
- Vascular damage in systemic lupus erythematosus.Nature reviews. Nephrology · 2024Review
- Comprehensive analysis of IRF8-related genes and immune characteristics in lupus nephritis.Frontiers in pharmacology · 2024Article
- Anti-complement factor H (CFH) autoantibodies could delay pristane-induced lupus nephritis.Immunologic research · 2023Article
- Clinical research progress of novel biologics for the treatment of lupus nephritis.Clinical and experimental medicine · 2023Review
- Immune podocytes in the immune microenvironment of lupus nephritis (Review).Molecular medicine reports · 2023Review
- New insights into the immune functions of podocytes: the role of complement.Molecular and cellular pediatrics · 2023Review
- Low-molecular weight inhibitors of the alternative complement pathway.Immunological reviews · 2023Review
- Kidney diseases.Immunological reviews · 2023Review
- Dysregulation of complement factor H in juvenile-onset systemic lupus erythematosus patients.Archives of rheumatology · 2022Article
- Intertwined pathways of complement activation command the pathogenesis of lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022Review
- The Rational Use of Complement Inhibitors in Kidney Diseases.Kidney international reports · 2022Review
- Comparison of Complement Pathway Activation in Autoimmune Glomerulonephritis.Kidney international reports · 2022Article
- Genetic analysis of CFH and MCP in Egyptian patients with immune-complex proliferative glomerulonephritis.Frontiers in immunology · 2022Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Complement factor H (CfH) is a key regulator of the alternative pathway, and its presence on mouse platelets and podocytes allows the processing of immune complexes. Because of the role of immune complexes in the pathophysiology of lupus nephritis, we studied the role of CfH in the development of nephritis in MRL-lpr mice, an animal model of lupus. At 12 weeks, CfH-deficient MRL-lpr mice had significantly more albuminuria and higher BUN levels than MRL-lpr controls. Cfh-deficient MRL-lpr mice also experienced earlier mortality: at 14 weeks, 6 of 9 CfH-deficient MRL-lpr mice had died of renal failure, whereas all 11 littermate CfH-sufficient MRL-lpr mice were alive (P ≤ 0.001). Histologically, CfH-deficient MRL-lpr mice developed severe diffuse lupus nephritis by 12 weeks (glomerulonephritis scores of 2.6 ± 0.4 versus 0.4 ± 0.2 in littermate controls, P = 0.001). Similar to other CfH-deficient mouse models on nonautoimmune backgrounds, immunofluorescence staining showed extensive linear C3 staining along glomerular capillary walls. IgG was present in the mesangium and peripheral capillary walls along with excessive infiltration of macrophages and neutrophils. Ultrastructurally, there were subendothelial and subepithelial immune deposits and extensive podocyte foot process effacement. In summary, the loss of CfH accelerates the development of lupus nephritis and recapitulates the functional and structural features of the human disease. This illustrates the critical role of complement regulation and metabolism of immune complexes in the pathogenesis of lupus nephritis.
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