ArticleKidney international2019
Glomerular membrane attack complex is not a reliable marker of ongoing C5 activation in lupus nephritis.
Article in Kidney international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
- Biomarkers in the Management of Complement-Mediated Kidney Diseases in the Era of Complement Therapeutics.Clinical journal of the American Society of Nephrology : CJASN · 2026Review
- Establishment of a Time-Resolved Fluoroimmunoassay for sC5b-9 and Validation in Lupus Nephritis.Journal of fluorescence · 2026Article
- A novel fusion protein reduces kidney complement in experimental C3 glomerulopathy.Clinical and experimental immunology · 2026Article
- 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
- Molecular and Cellular Mediators of Renal Fibrosis in Lupus Nephritis.International journal of molecular sciences · 2025Review
- The utility of CXCL13 and circulating CXCR5Frontiers in immunology · 2025Article
- Urinary sC5b-9 is Better Linked to Albuminuria Than to Intrarenal Inflammation in Common Kidney Disease.Kidney international reports · 2024Article
- Apical tubular complement activation and the loss of kidney function in proteinuric kidney diseases.Clinical kidney journal · 2024Review
- Article
- Microvascular C5b-9 deposition in non-lesional skin in patients with SLE and its correlation with active lupus nephritis: a prospective observational study.Lupus science & medicine · 2023Observational
- C3-dependent effector functions of complement.Immunological reviews · 2023Review
- A Histology-Guided Approach to the Management of Patients with Lupus Nephritis: Are We There Yet?Biomedicines · 2022Review
- The Rational Use of Complement Inhibitors in Kidney Diseases.Kidney international reports · 2022Review
- Urinary C5b-9 as a Prognostic Marker in IgA Nephropathy.Journal of clinical medicine · 2022Article
- Membrane attack complex (MAC) deposition in renal tubules is associated with interstitial fibrosis and tubular atrophy: a pilot study.Lupus science & medicine · 2022Article
- Eculizumab and Complement Activation in Anti-glomerular Basement Membrane Disease.Kidney international reports · 2021Article
- Natural antibody and complement activation characterize patients with idiopathic nephrotic syndrome.American journal of physiology. Renal physiology · 2021Article
- Expanding the Role of Complement Therapies: The Case for Lupus Nephritis.Journal of clinical medicine · 2021Review
- Complement activity is regulated in C3 glomerulopathy by IgG-factor H fusion proteins with and without properdin targeting domains.Kidney international · 2021Article
- The Spectrum of C4d Deposition in Renal Biopsies of Lupus Nephritis Patients.Frontiers in immunology · 2021Article
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Complement plays an important role in the pathogenesis of lupus nephritis (LN). With the emergence of therapeutic complement inhibition, there is a need to identify patients in whom complement-driven inflammation is a major cause of kidney injury in LN. Clinical and histopathological data were obtained retrospectively from 57 biopsies with class III, IV, and V LN. Biopsies were stained for complement components C9, C5b-9, C3c, and C3d and for the macrophage marker CD68. C9 and C5b-9 staining were highly correlated (r = 0.92 in the capillary wall). C5b-9 staining was detected in the mesangium and/or capillary wall of both active and chronic proliferative LN in all but one biopsy and in the capillary wall of class V LN in all biopsies. C5b-9 staining intensity in the tubular basement membrane correlated with markers of tubulointerstitial damage, and more intense capillary wall C5b-9 staining was significantly associated with nonresponse to conventional treatment. Glomerular C5b-9 staining intensity did not differ between active and chronic disease; in contrast, C3c and CD68 staining were associated with active disease. Evaluation of serial biopsies and comparison of staining in active and chronic LN demonstrated that C5b-9 staining persisted for months to years. These results suggest that C5b-9 staining is almost always present in LN, resolves slowly, and is not a reliable marker of ongoing glomerular C5 activation. This limits the utility of C5b-9 staining to identify patients who are most likely to benefit from C5 inhibition.
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