Evidence map›Paper›PMID 28624979›Full record

ReviewPediatric nephrology (Berlin, Germany)2018

New insights into the pathogenesis of IgA nephropathy.

See Cheng Yeo, Chee Kay Cheung, Jonathan Barratt

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 9 pooled it
8.9field-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

80 citing papers in PubMed, 9 syntheses or guidelines pooled it, 162 citations in OpenAlex.

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  6. Immunosuppressive therapy for IgA nephropathy in children.The Cochrane database of systematic reviews · 2024
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20 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

3 authors at 2 institutions in 2 countries.

See Cheng YeoDepartment of Renal Medicine, Tan Tock Seng Hospital, Singapore, Singapore.
Chee Kay CheungDepartment of Infection, Immunity and Inflammation, University of Leicester, University Road, Leicester, LE1 7RH, UK.
Jonathan BarrattDepartment of Infection, Immunity and Inflammation, University of Leicester, University Road, Leicester, LE1 7RH, UK. jb81@le.ac.uk.ORCID 0000-0002-9063-7229
University of Leicester · GBTan Tock Seng Hospital · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgA nephropathy is the most common form of glomerulonephritis in many parts of the world and remains an important cause of end-stage renal disease. Current evidence suggests that IgA nephropathy is not due to a single pathogenic insult, but rather the result of multiple sequential pathogenic "hits". An abnormally increased level of circulating poorly O-galactosylated IgA1 and the production of O-glycan-specific antibodies leads to the formation of IgA1-containing immune complexes, and their subsequent mesangial deposition results in inflammation and glomerular injury. While this general framework has formed the foundation of our current understanding of the pathogenesis of IgA nephropathy, much work is ongoing to try to precisely define the genetic, epigenetic, immunological, and molecular basis of IgA nephropathy. In particular, the precise origin of poorly O-galactosylated IgA1 and the inciting factors for the production of O-glycan-specific antibodies continue to be intensely evaluated. The mechanisms responsible for mesangial IgA1 deposition and subsequent renal injury also remain incompletely understood. In this review, we summarize the current understanding of the key steps involved in the pathogenesis of IgA nephropathy. It is hoped that further advances in our understanding of this common glomerulonephritis will lead to novel diagnostic and prognostic biomarkers, and targeted therapies to ameliorate disease progression.

Indexed as

Glomerulonephritis, IGAHumansImmunoglobulin AKidneyImmunoglobulin AIgA1IgA nephropathyImmune complexesO-galactosylationPathogenesis

Identifiers

PMID28624979
PMCPMC5861174
OpenAlexW2625366743

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.