Evidence map›Paper›PMID 26459770›Full record

ReviewClinical and experimental immunology2016

Immunology of membranous nephropathy: from animal models to humans.

R A Sinico, N Mezzina, B Trezzi, G M Ghiggeri, A Radice

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical and experimental immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 86 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

R A SinicoClinical Immunology Unit and Renal Unit, Institute of Microbiology, Azienda Ospedaliera Ospedale San Carlo Borromeo.
N MezzinaClinical Immunology Unit and Renal Unit, Institute of Microbiology, Azienda Ospedaliera Ospedale San Carlo Borromeo.
B TrezziAzienda Ospedaliera Polo Universitario Luigi Sacco, Rheumatology Unit, Milano, Italy.
G M GhiggeriDivision of Nephrology, Dialysis, and Transplantation, Scientific Institute for Research and Health Care (IRCCS), Istituto Giannina Gaslini, Genoa, Italy.
A RadiceClinical Immunology Unit and Renal Unit, Institute of Microbiology, Azienda Ospedaliera Ospedale San Carlo Borromeo.
Azienda Ospedaliera Ospedale San Carlo Borromeo · ITIstituto Giannina Gaslini · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Membranous nephropathy (MN), the leading cause of nephrotic syndrome in adults, is characterized by the deposition of subepithelial immune deposits that consist mainly of immunoglobulin (Ig)G and complement. Most of the cases are primary or idiopathic (iMN), while only approximately 25% of the cases are secondary to some known disease such as systemic lupus erythematosus, hepatitis B, drugs and malignancies. Most of our knowledge on the pathogenesis of iMN has relied upon old experimental models (i.e. Heymann nephritis) that have shown that immune deposits are formed in situ by the reaction of autoantibodies against the respective podocyte antigen. Recent findings indicate that podocyte proteins also act as an autoantigen in human iMN. The M-type phospholipase A2 receptor (PLA2R) has been identified as the main target antigen, as it can be found in approximately 70% of iMN patients but only rarely in other glomerulonephritides. Podocytes damage in the experimental model of Heymann nephritis is complement-mediated. In humans, the presence of complement within the subepithelial deposits is well established, but IgG4, which does not activate complement by classical or alternative pathways, represents the predominant subclass of IgG anti-PLA2R. Some evidence suggests that IgG4 anti-PLA2R autoantibodies can bind mannan-binding lectin (MBL) and activate the lectin complement pathway. A genetic background for iMN has been demonstrated by genome-wide association studies that have shown highly significant associations of the PLA2R1 and the human leucocyte antigen (HLA)-DQA1 loci with iMN. In addition to their diagnostic value, anti-PLA2R antibodies may be useful to monitor disease activity and predict response to treatment.

Indexed as

AdultAnimalsAntibodies, Anti-IdiotypicAutoantibodiesAutoantigensComplement System ProteinsDisease Models, AnimalGlomerulonephritis, MembranousHLA-DQ alpha-ChainsHumansPodocytesReceptors, Phospholipase A2Antibodies, Anti-Idiotypicanti-IgGAutoantibodiesAutoantigensComplement System ProteinsHLA-DQA1 antigenHLA-DQ alpha-ChainsPLA2R1 protein, humanReceptors, Phospholipase A2anti-PLA2R antibodymembranous nephropathypodocytesubepithelial deposits IgG4

Identifiers

PMID26459770
PMCPMC4711165
OpenAlexW1913814900

What OpenQuestion holds

Textmetadata
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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.