Evidence map›Paper›PMID 25694468›Full record

ReviewJournal of the American Society of Nephrology : JASN2015

Current Understanding of the Role of Complement in IgA Nephropathy.

Nicolas Maillard, Robert J Wyatt, Bruce A Julian, Krzysztof Kiryluk, Ali Gharavi, Veronique Fremeaux-Bacchi, Jan Novak

Open access · greenAbstract readReview
In one paragraph

Review in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
198citing papers in PubMed, 4 pooled it
15.8field-weighted citation impact, top 1% of its field
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

198 citing papers in PubMed, 4 syntheses or guidelines pooled it, 334 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Non-immunosuppressive treatment for IgA nephropathy.The Cochrane database of systematic reviews · 2024
    Pooled it
  4. Immunosuppressive agents for treating IgA nephropathy.The Cochrane database of systematic reviews · 2020
    Pooled it
  5. Trial
  6. Trial
  7. A Rare Genetic Defect ofFrontiers in immunology · 2019
    Trial
  8. Article
  9. Article
  10. Article
  11. Association of Complement Genetics with Outcomes in IgA Nephropathy.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Article
  12. Review
  13. Article
  14. Review
  15. The endothelium response to kidney injury.Nature reviews. Nephrology · 2026
    Review
  16. New prognostic markers for IgA nephropathy in children.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  17. Article
  18. Review
  19. Article
  20. Article

138 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 2 countries.

Nicolas MaillardUniversity of Alabama at Birmingham, Departments of Microbiology and Medicine, Birmingham, Alabama; Université Jean Monnet, Groupe sur l'immunité des Muqueuses et Agents Pathogènes, St. Etienne, Pôle de Recherche et d'Enseignement Supérieur, Université de Lyon, Lyon, France;
Robert J WyattUniversity of Tennessee Health Science Center and Children's Foundation Research at the Le Bonheur Children's Hospital, Memphis, Tennessee;
Bruce A JulianUniversity of Alabama at Birmingham, Departments of Microbiology and Medicine, Birmingham, Alabama;
Krzysztof KirylukColumbia University, Department of Medicine, New York, New York; and.
Ali GharaviColumbia University, Department of Medicine, New York, New York; and.
Veronique Fremeaux-BacchiUnité Mixte de Recherche en Santé 1138, Team "Complement and Diseases," Cordeliers Research Center, Paris, France.
Jan NovakUniversity of Alabama at Birmingham, Departments of Microbiology and Medicine, Birmingham, Alabama; jannovak@uab.edu.
University of Alabama at Birmingham · USColumbia University · USCentre de Recherche des Cordeliers · FRUniversity of Tennessee Health Science Center · US

Funding

Elucidating IgA Nephropathy through Genetic Studies of IgA1 GlycosylationR01DK082753 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GHARAVI, ALI G, NOVAK, JAN · 2009 to 2024
$8.7M
Molecular Basis of Pathogenicity of IgA1-containing Immune ComplexesR01DK078244 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JAN NOVAK · 2007 to 2026
$6.0M
Analytical tools for the analysis of clustered O-glycans in clinical samplesR01GM098539 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RENFROW, MATTHEW B · 2011 to 2019
$2.7M
Quantitative Genetics of Defective IgA1 Glycosylation in IgA NephropathyK23DK090207 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KIRYLUK, KRZYSZTOF · 2011 to 2014
$729k
Molecular Basis of Pathogenicity of IgA1-containing Immune ComplexesR56DK078244 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI NOVAK, JAN · 2012 to 2012
$92k
NIDDK NIH HHS DK078244NIDDK NIH HHS DK082753NIDDK NIH HHS DK090207NIDDK NIH HHS K23 DK090207NIDDK NIH HHS R01 DK078244NIDDK NIH HHS R01 DK082753NIDDK NIH HHS R56 DK078244NIGMS NIH HHS GM098539NIGMS NIH HHS R01 GM098539
6 · The paper itself

Abstract

Complement activation has a role in the pathogenesis of IgA nephropathy, an autoimmune disease mediated by pathogenic immune complexes consisting of galactose-deficient IgA1 bound by antiglycan antibodies. Of three complement-activation pathways, the alternative and lectin pathways are involved in IgA nephropathy. IgA1 can activate both pathways in vitro, and pathway components are present in the mesangial immunodeposits, including properdin and factor H in the alternative pathway and mannan-binding lectin, mannan-binding lectin-associated serine proteases 1 and 2, and C4d in the lectin pathway. Genome-wide association studies identified deletion of complement factor H-related genes 1 and 3 as protective against the disease. Because the corresponding gene products compete with factor H in the regulation of the alternative pathway, it has been hypothesized that the absence of these genes could lead to more potent inhibition of complement by factor H. Complement activation can take place directly on IgA1-containing immune complexes in circulation and/or after their deposition in the mesangium. Notably, complement factors and their fragments may serve as biomarkers of IgA nephropathy in serum, urine, or renal tissue. A better understanding of the role of complement in IgA nephropathy may provide potential targets and rationale for development of complement-targeting therapy of the disease.

Indexed as

Genetic Predisposition to DiseaseComplement ActivationComplement System ProteinsComprehensionFemaleGene Expression RegulationGenome-Wide Association StudyGlomerulonephritis, IGAHumansImmunoglobulin AMalePrognosisRisk FactorsRoleSensitivity and SpecificitySeverity of Illness IndexComplement System ProteinsImmunoglobulin AcomplementIgA nephropathyimmune complexes

Identifiers

PMID25694468
PMCPMC4483595
OpenAlexW2017568050

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.