Evidence map›Paper›PMID 40717085›Full record

ArticleMolecular medicine (Cambridge, Mass.)2025

Evaluating the usefulness of C5 and C5AR1 as genetic biomarkers of IgA-mediated vasculitis.

Joao Carlos Batista-Liz, Vanesa Calvo-Río, María Sebastián Mora-Gil, María Teresa Leonardo, Ana Cristina Peñalba, Luis Martín-Penagos, Javier Narváez, Belén Sevilla-Pérez, José Luis Callejas-Rubio, Ligia Gabrie and 14 more

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

24 authors.

Joao Carlos Batista-LizImmunopathology Group, Fundación Instituto de Investigación Marqués de Valdecilla, Santander, 39011, Spain.
Vanesa Calvo-RíoImmunopathology Group, Fundación Instituto de Investigación Marqués de Valdecilla, Santander, 39011, Spain.
María Sebastián Mora-GilImmunopathology Group, Fundación Instituto de Investigación Marqués de Valdecilla, Santander, 39011, Spain.
María Teresa LeonardoDivision of Paediatrics, Hospital Universitario Marqués de Valdecilla, Santander, 39008, Spain.
Ana Cristina PeñalbaDivision of Paediatrics, Hospital Universitario Marqués de Valdecilla, Santander, 39008, Spain.
Luis Martín-PenagosImmunopathology Group, Fundación Instituto de Investigación Marqués de Valdecilla, Santander, 39011, Spain.
Javier NarváezDivision of Rheumatology, Hospital Universitario de Bellvitge, L'Hospitalet de Llobregat, 08907, Spain.
Belén Sevilla-PérezDivision of Paediatrics, Hospital Universitario Clínico San Cecilio, Granada, 18007, Spain.
José Luis Callejas-RubioSystemic Autoimmune Disease Unit, Hospital Universitario Clínico San Cecilio, Instituto de Investigación Biosanitaria Ibs.GRANADA, Granada, 18007, Spain.
Ligia GabrieImmunopathology Group, Fundación Instituto de Investigación Marqués de Valdecilla, Santander, 39011, Spain.
Rafael Gálvez SánchezImmunopathology Group, Fundación Instituto de Investigación Marqués de Valdecilla, Santander, 39011, Spain.
Luis Caminal-MonteroInternal Medicine Department, Hospital Universitario Central de Asturias, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Oviedo, 33011, Spain.
Paz ColladoDivision of Rheumatology, Hospital Universitario Severo Ochoa, Leganés, 28914, Spain.
María José Rodríguez VallsDivision of Rheumatology, Hospital General de Jerez, Jerez de La Frontera, 11407, Spain.
Diego de ArgilaDivision of Dermatology, Hospital Universitario de La Princesa, Madrid, 28006, Spain.
Patricia Quiroga-ColinaDivision of Rheumatology, IIS-Princesa, Universidad Autónoma de Madrid, Hospital Universitario de La Princesa, Madrid, 28006, Spain.
Esther Francisca Vicente-RabanedaDivision of Rheumatology, IIS-Princesa, Universidad Autónoma de Madrid, Hospital Universitario de La Princesa, Madrid, 28006, Spain.
Esteban RubioDepartment of Rheumatology, Hospital Universitario Virgen del Rocío, Sevilla, 41013, Spain.
Manuel León LuqueDepartment of Rheumatology, Hospital Universitario Virgen del Rocío, Sevilla, 41013, Spain.
Juan María Blanco-MadrigalDivision of Rheumatology, Hospital Universitario de Basurto, Bilbao, 48013, Spain.
Eva Galíndez-AgirregoikoaDivision of Rheumatology, Hospital Universitario de Basurto, Bilbao, 48013, Spain.
Ricardo Blanco *Immunopathology Group, Fundación Instituto de Investigación Marqués de Valdecilla, Santander, 39011, Spain.
Verónica Pulito-Cueto *Immunopathology Group, Fundación Instituto de Investigación Marqués de Valdecilla, Santander, 39011, Spain. veronica_pulito_cueto@hotmail.com.
Raquel López-Mejías *Immunopathology Group, Fundación Instituto de Investigación Marqués de Valdecilla, Santander, 39011, Spain. rlopezmejias78@gmail.com.

Funding

Instituto de Investigación Marqués de Valdecilla NVAL2302Instituto de Salud Carlos III CPII21/00004Instituto de Salud Carlos III FI22/00020
6 · The paper itself

Abstract

backgroundIgA-mediated vasculitis (IgAV) is a complex inflammatory disease. Unravelling its genetic background would allow us to identify genetic biomarkers that may be used as additional tools in its daily management, helping to solve the clinical challenge that this vasculitis entails. C5 is a potent immune mediator that is proteolytically processed to generate C5a, a potent anaphylatoxin that exerts its function via C5aR1. C5 downstream variants (rs3761847 and rs10818488) have been recently related to IgAV pathogenesis. Additionally, C5a and C5aR1 dysregulation contributes to the development of inflammatory diseases, and, particularly, elevated C5a plasma levels have been observed in IgAV patients in the acute stage. Accordingly, we aimed to evaluate the influence of C5 and C5AR1 on the pathophysiology of IgAV.

methodsEight C5 (rs10760128, rs74971050, rs4310279, rs7868761, rs10818495, rs10156396, rs3815467, and rs16910280) and three C5AR1 (rs10853784, rs11673071, and rs11670789) tag variants were genotyped in 342 Caucasian IgAV patients and 723 ethnically matched healthy controls.

resultsNo statistically significant differences were observed when C5 and C5AR1 frequencies were compared between IgAV patients and healthy controls. Likewise, similar C5 and C5AR1 frequencies were observed amongst IgAV patients stratified according to IgAV severity (presence/absence of nephritis). Furthermore, no C5 and C5AR1 differences were disclosed when IgAV patients were stratified according to demographic and clinical IgAV characteristics other than nephritis (age at disease onset, presence/absence of joint and gastrointestinal manifestations) and sex.

conclusionsOur results suggest that C5 and C5AR1 are not related to IgAV pathogenesis and, therefore, these genes may not be useful as IgAV genetic biomarkers.

Indexed as

Complement C5Immunoglobulin AReceptor, Anaphylatoxin C5aVasculitisAdolescentAdultBiomarkersCase-Control StudiesFemaleGene FrequencyGenetic MarkersGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedBiomarkersC5AR1 protein, humanComplement C5Genetic MarkersImmunoglobulin AReceptor, Anaphylatoxin C5aBiomarkersC5C5AR1GeneticsIgA Vasculitis

Identifiers

PMID40717085
PMCPMC12296620

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.