Evidence map›Paper›PMID 38362118›Full record

ReviewFrontiers in nephrology2023

The role of BAFF and APRIL in IgA nephropathy: pathogenic mechanisms and targeted therapies.

Chee Kay Cheung, Jonathan Barratt, Adrian Liew, Hong Zhang, Vladimir Tesar, Richard Lafayette

Open access · diamondAbstract readReview
In one paragraph

Review in Frontiers in nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 3 pooled it
21.4field-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

60 citing papers in PubMed, 3 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. IgA2Cell reports. Medicine · 2025
    Trial
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  20. Kidney Disease as a Driver of Immunosenescence: Mechanisms and Potential Interventions.Journal of the American Society of Nephrology : JASN · 2026
    Review
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 at 6 institutions in 5 countries.

Chee Kay CheungDivision of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom.
Jonathan BarrattDivision of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom.
Adrian LiewThe Kidney & Transplant Practice, Mount Elizabeth Novena Hospital, Singapore.
Hong ZhangRenal Division in the Department of Medicine, Peking University First Hospital, Beijing, China.
Vladimir TesarDepartment of Nephrology, First School of Medicine and General University Hospital, Charles University, Prague, Czechia.
Richard LafayetteDepartment of Medicine, Stanford University, Stanford, CA, United States.
Charles University · CZMount Elizabeth Novena Hospital · SGNational Health Service · GBPeking University First Hospital · CNStanford University · USUniversity of Leicester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoglobulin A nephropathy (IgAN), characterized by mesangial deposition of galactose-deficient-IgA1 (Gd-IgA1), is the most common biopsy-proven primary glomerulonephritis worldwide. Recently, an improved understanding of its underlying pathogenesis and the substantial risk of progression to kidney failure has emerged. The "four-hit hypothesis" of IgAN pathogenesis outlines a process that begins with elevated circulating levels of Gd-IgA1 that trigger autoantibody production. This results in the formation and deposition of immune complexes in the mesangium, leading to inflammation and kidney injury. Key mediators of the production of Gd-IgA1 and its corresponding autoantibodies are B-cell activating factor (BAFF), and A proliferation-inducing ligand (APRIL), each playing essential roles in the survival and maintenance of B cells and humoral immunity. Elevated serum levels of both BAFF and APRIL are observed in patients with IgAN and correlate with disease severity. This review explores the complex pathogenesis of IgAN, highlighting the pivotal roles of BAFF and APRIL in the interplay between mucosal hyper-responsiveness, B-cell activation, and the consequent overproduction of Gd-IgA1 and its autoantibodies that are key features in this disease. Finally, the potential therapeutic benefits of inhibiting BAFF and APRIL in IgAN, and a summary of recent clinical trial data, will be discussed.

Indexed as

a proliferation-inducing ligand APRILataciceptB-cell activating factor BAFFdual inhibitionIgA nephropathy

Identifiers

PMID38362118
PMCPMC10867227
OpenAlexW4391444142

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.