Evidence map›Paper›PMID 24442210›Full record

ReviewSeminars in immunopathology2014

New insights into the pathogenesis of IgA nephropathy.

Jürgen Floege, Ivan C Moura, Mohamed R Daha

Abstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

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  9. GABA signaling enforces intestinal germinal center B cell differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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 3 institutions in 3 countries.

Jürgen FloegeDivision of Nephrology, RWTH University Hospital Aachen, 52057, Aachen, Germany, jfloege@ukaachen.de.
Ivan C Moura
Mohamed R Daha
Leiden University Medical Center · NLSorbonne Paris Cité · FRUniversitätsklinikum Aachen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgA nephropathy (IgAN) is the most common diagnosis amongst primary glomerular diseases in most countries where renal biopsies are regularly performed. Only a fraction of these patients is at high risk of losing glomerular filtration rate (GFR) in particular those with high grade proteinuria, uncontrolled hypertension or already impaired GFR at diagnosis, and those with renal scars in the renal biopsy. Genetic modifiers of IgAN onset and/or course are emerging. Spontaneous animal models of IgAN are problematic given considerable species differences between the rodent and human IgA system. However, new transgenic models help to better understand the pathogenesis. A key pathogenetic role appears to be played by underglycated IgA1 as well as autoantibodies to these IgA glycoforms and IgA receptors such as CD89 and transferrin receptor 1. Once IgA and/or IgA-containing immune complexes are deposited or formed in the mesangium, secondary effector mechanisms become important including complement activation, release of mesangial growth factors (in particular platelet-derived growth factor), and finally non-IgAN-specific events that culminate in glomerular and subsequently renal tubulointerstitial scaring. Here, we review these processes and describe potential novel therapeutic targets in IgAN.

Indexed as

Antigens, CDComplement System ProteinsGlomerular Filtration RateGlomerulonephritis, IGAHumansImmunoglobulin AKidneyPlatelet-Derived Growth FactorReceptors, FcReceptors, TransferrinAntigens, CDCD71 antigenComplement System ProteinsFc(alpha) receptorImmunoglobulin APlatelet-Derived Growth FactorReceptors, FcReceptors, Transferrin

Identifiers

PMID24442210
OpenAlexW1967721721

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.