Evidence map›Paper›PMID 26850635›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

IgA1 Protease Treatment Reverses Mesangial Deposits and Hematuria in a Model of IgA Nephropathy.

Sebastian M Lechner, Lilia Abbad, Erwan Boedec, Christina Papista, Marie-Bénédicte Le Stang, Christelle Moal, Julien Maillard, Agnès Jamin, Julie Bex-Coudrat, Yong Wang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
5.3field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.

  1. Pooled it
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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

14 authors at 7 institutions in 2 countries.

Sebastian M LechnerNational French Institute of Health and Medical Research (INSERM) Unit 1149, Center of Research on Inflammation, Paris, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France;
Lilia AbbadNational French Institute of Health and Medical Research (INSERM) Unit 1149, Center of Research on Inflammation, Paris, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France;
Erwan BoedecNational French Institute of Health and Medical Research (INSERM) Unit 1149, Center of Research on Inflammation, Paris, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France;
Christina PapistaNational French Institute of Health and Medical Research (INSERM) Unit 1149, Center of Research on Inflammation, Paris, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France;
Marie-Bénédicte Le StangNational French Institute of Health and Medical Research (INSERM) Unit 1149, Center of Research on Inflammation, Paris, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France;
Christelle MoalNational French Institute of Health and Medical Research (INSERM) Unit 1149, Center of Research on Inflammation, Paris, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France;
Julien MaillardNational French Institute of Health and Medical Research (INSERM) Unit 1149, Center of Research on Inflammation, Paris, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France;
Agnès JaminNational French Institute of Health and Medical Research (INSERM) Unit 1149, Center of Research on Inflammation, Paris, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France;
Julie Bex-CoudratNational French Institute of Health and Medical Research (INSERM) Unit 1149, Center of Research on Inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France;
Yong WangShire, Bioprocess Development and Discovery Biology and Translational Research, Lexington, Massachusetts; and.
Aiqun LiShire, Bioprocess Development and Discovery Biology and Translational Research, Lexington, Massachusetts; and.
Paolo G V MartiniShire, Bioprocess Development and Discovery Biology and Translational Research, Lexington, Massachusetts; and.
Renato C MonteiroNational French Institute of Health and Medical Research (INSERM) Unit 1149, Center of Research on Inflammation, Paris, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France; Immunology Department, Bichat Hospital, Paris Public Assistance Hospitals, Department of Hospital and University (DHU) Fire, Paris, France renato.monteiro@inserm.fr laureline.berthelot@inserm.fr.
Laureline BerthelotNational French Institute of Health and Medical Research (INSERM) Unit 1149, Center of Research on Inflammation, Paris, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France; renato.monteiro@inserm.fr laureline.berthelot@inserm.fr.
Centre National de la Recherche Scientifique · FRTakeda (United States) · USCentre de Recherche sur l'Inflammation · FRDélégation Paris 7 · FRInserm · FRLaboratoire Excell · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgA nephropathy (IgAN), characterized by mesangial IgA1 deposits, is a leading cause of renal failure worldwide. IgAN pathogenesis involves circulating hypogalactosylated IgA1 complexed with soluble IgA Fc receptor I (sCD89) and/or anti-hypogalactosylated-IgA1 autoantibodies, but no specific treatment is available for IgAN. The absence of IgA1 and CD89 homologs in the mouse has precluded in vivo proof-of-concept studies of specific therapies targeting IgA1. However, the α1KI‑CD89Tg mouse model of IgAN, which expresses human IgA1 and human CD89, allows in vivo testing of recombinant IgA1 protease (IgA1‑P), a bacterial protein that selectively cleaves human IgA1. Mice injected with IgA1‑P (1-10 mg/kg) had Fc fragments of IgA1 in both serum and urine, associated with a decrease in IgA1-sCD89 complexes. Levels of mesangial IgA1 deposits and the binding partners of these deposits (sCD89, transferrin receptor, and transglutaminase 2) decreased markedly 1 week after treatment, as did the levels of C3 deposition, CD11b(+) infiltrating cells, and fibronectin. Antiprotease antibodies did not significantly alter IgA1‑P activity. Moreover, hematuria consistently decreased after treatment. In conclusion, IgA1‑P strongly diminishes human IgA1 mesangial deposits and reduces inflammation, fibrosis, and hematuria in a mouse IgAN model, and therefore may be a plausible treatment for patients with IgAN.

Indexed as

AnimalsDisease Models, AnimalGlomerular MesangiumGlomerulonephritis, IGAHematuriaImmunoglobulin AMiceSerine EndopeptidasesIgA-specific serine endopeptidaseImmunoglobulin ASerine EndopeptidasesglomerulonephritisIgA nephropathyimmune complexesimmunologypathology

Identifiers

PMID26850635
PMCPMC5004657
OpenAlexW2258657103

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.