ArticleClinical and experimental immunology2016
Serum properdin consumption as a biomarker of C5 convertase dysregulation in C3 glomerulopathy.
Article in Clinical and experimental immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Pooled it
- A novel fusion protein reduces kidney complement in experimental C3 glomerulopathy.Clinical and experimental immunology · 2026Article
- Stage II of Chronic Kidney Disease-A Tipping Point in Disease Progression?Biomedicines · 2022Article
- A clinical approach to children with C3 glomerulopathy.Pediatric nephrology (Berlin, Germany) · 2022Review
- Severe COVID-19 is associated with hyperactivation of the alternative complement pathway.The Journal of allergy and clinical immunology · 2022Article
- Challenges in diagnostic testing of nephritic factors.Frontiers in immunology · 2022Review
- Elevated Expression Levels of Lung Complement Anaphylatoxin, Neutrophil Chemoattractant Chemokine IL-8, and RANTES in MERS-CoV-Infected Patients: Predictive Biomarkers for Disease Severity and Mortality.Journal of clinical immunology · 2021Article
- Complement activity is regulated in C3 glomerulopathy by IgG-factor H fusion proteins with and without properdin targeting domains.Kidney international · 2021Article
- pH-responsive antibodies for therapeutic applications.Journal of biomedical science · 2021Review
- Immunological features of patients affected by Barraquer-Simons syndrome.Orphanet journal of rare diseases · 2020Article
- The role of properdin in complement-mediated renal diseases: a new player in complement-inhibiting therapy?Pediatric nephrology (Berlin, Germany) · 2019Article
- Nephritic Factors: An Overview of Classification, Diagnostic Tools and Clinical Associations.Frontiers in immunology · 2019Review
- Properdin: A multifaceted molecule involved in inflammation and diseases.Molecular immunology · 2018Review
- Increased serum protein levels by Yuanshi Shengmai Chenggu Tablet in treatment of avascular osteonecrosis of the femoral head.Molecular medicine reports · 2018Article
- Unraveling the Molecular Mechanisms Underlying Complement Dysregulation by Nephritic Factors in C3G and IC-MPGN.Frontiers in immunology · 2018Article
- Complement C3-Targeted Therapy: Replacing Long-Held Assertions with Evidence-Based Discovery.Trends in immunology · 2017Article
- Properdin: a tightly regulated critical inflammatory modulator.Immunological reviews · 2016Review
- Testing the Activity of Complement Convertases in Serum/Plasma for Diagnosis of C4NeF-Mediated C3 Glomerulonephritis.Journal of clinical immunology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Properdin (P) stabilizes the alternative pathway (AP) convertases, being the only known positive regulator of the complement system. In addition, P is a pattern recognition molecule able to initiate directly the AP on non-self surfaces. Although P deficiencies have long been known to be associated with Neisseria infections and P is often found deposited at sites of AP activation and tissue injury, the potential role of P in the pathogenesis of complement dysregulation-associated disorders has not been studied extensively. Serum P levels were measured in 49 patients with histological and clinical evidence of C3 glomerulopathy (C3G). Patients were divided into two groups according to the presence or absence of C3 nephritic factor (C3NeF), an autoantibody that stabilizes the AP C3 convertase. The presence of this autoantibody results in a significant reduction in circulating C3 (P < 0·001) and C5 levels (P < 0·05), but does not alter factor B, P and sC5b-9 levels. Interestingly, in our cohort, serum P levels were low in 17 of the 32 C3NeF-negative patients. This group exhibited significant reduction of C3 (P < 0·001) and C5 (P < 0·001) and increase of sC5b-9 (P < 0·001) plasma levels compared to the control group. Also, P consumption was correlated significantly with C3 (r = 0·798, P = 0·0001), C5 (r = 0·806, P < 0·0001), sC5b-9 (r = -0·683, P = 0·043) and a higher degree of proteinuria (r = -0·862, P = 0·013). These results illustrate further the heterogeneity among C3G patients and suggest that P serum levels could be a reliable clinical biomarker to identify patients with underlying surface AP C5 convertase dysregulation.
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