Evidence map›Paper›PMID 39232245›Full record

ReviewNature reviews. Nephrology2025

The pathogenesis of IgA nephropathy and implications for treatment.

Chee Kay Cheung, Suceena Alexander, Heather N Reich, Haresh Selvaskandan, Hong Zhang, Jonathan Barratt

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed, 6 pooled it
–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

135 citing papers in PubMed, 6 syntheses or guidelines pooled it.

  1. Pooled it
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  7. Trial
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  12. Sarsasapogenin Preserves Podocyte Integrity and Attenuates Renal Injury in Experimental IgA Nephropathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  14. Review
  15. Article
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  19. Review
  20. IgA nephropathy management: what does the future hold?Kidney international supplements · 2026
    Review

75 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

6 authors.

Chee Kay CheungMayer IgA Nephropathy Laboratories, Department of Cardiovascular Sciences, University of Leicester, Leicester, UK. ckc15@leicester.ac.uk.
Suceena AlexanderDepartment of Nephrology, Christian Medical College, Vellore, India.
Heather N ReichDepartment of Medicine, Division of Nephrology, University of Toronto, University Health Network, Toronto, ON, Canada.
Haresh SelvaskandanMayer IgA Nephropathy Laboratories, Department of Cardiovascular Sciences, University of Leicester, Leicester, UK.
Hong ZhangRenal Division, Peking University First Hospital, Peking University Institute of Nephrology, Beijing, P. R. China.
Jonathan BarrattMayer IgA Nephropathy Laboratories, Department of Cardiovascular Sciences, University of Leicester, Leicester, UK. jb81@leicester.ac.uk.ORCID http://orcid.org/0000-0002-9063-7229

Funding

DBT-Wellcome Trust India Alliance IA/CPHS/22/1/506541
6 · The paper itself

Abstract

IgA nephropathy (IgAN) is a common form of primary glomerulonephritis and represents an important cause of chronic kidney disease globally, with observational studies indicating that most patients are at risk of developing kidney failure within their lifetime. Several research advances have provided insights into the underlying disease pathogenesis, framed by a multi-hit model whereby an increase in circulating IgA1 that lacks galactose from its hinge region - probably derived from the mucosal immune system - is followed by binding of specific IgG and IgA antibodies, generating immune complexes that deposit within the glomeruli, which triggers inflammation, complement activation and kidney damage. Although treatment options are currently limited, new therapies are rapidly emerging that target different pathways, cells and mediators involved in the disease pathogenesis, including B cell priming in the gut mucosa, the cytokines APRIL and BAFF, plasma cells, complement activation and endothelin pathway activation. As more treatments become available, there is a realistic possibility of transforming the long-term outlook for many individuals with IgAN.

Indexed as

Glomerulonephritis, IGAB-Cell Activating FactorB-LymphocytesComplement ActivationHumansImmunoglobulin ATumor Necrosis Factor Ligand Superfamily Member 13B-Cell Activating FactorImmunoglobulin ATumor Necrosis Factor Ligand Superfamily Member 13

Identifiers

PMID39232245
PMCPMC7616674

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.