Evidence map›Paper›PMID 34459222›Full record

ArticleAmerican journal of physiology. Renal physiology2021

Natural antibody and complement activation characterize patients with idiopathic nephrotic syndrome.

Howard Trachtman, Jennifer Laskowski, Cameron Lee, Brandon Renner, Andrew Feemster, Samir Parikh, Sarah E Panzer, Weixiong Zhong, Paolo Cravedi, Chiara Cantarelli and 9 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.4field-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

33 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Dual anti-CD20/anti-CD38 therapy for severe recurrent FSGS with longitudinal anti-nephrin assessment.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Article
  5. Review
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  7. B-cell-targeting therapies in podocytopathies.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Role of local complement activation in kidney fibrosis and repair.The Journal of clinical investigation · 2025
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
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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

19 authors at 8 institutions in 3 countries.

Howard TrachtmanDepartment of Pediatrics, Langone Medical Center, New York University School of Medicine, New York, New York.
Jennifer LaskowskiDepartment of Medicine, Anschutz Medical Campus, University of Colorado School of Medicine, Aurora, Colorado.
Cameron LeeDepartment of Medicine, Anschutz Medical Campus, University of Colorado School of Medicine, Aurora, Colorado.
Brandon RennerDepartment of Medicine, Anschutz Medical Campus, University of Colorado School of Medicine, Aurora, Colorado.
Andrew FeemsterDepartment of Pediatrics, Langone Medical Center, New York University School of Medicine, New York, New York.
Samir ParikhDepartment of Internal Medicine, Ohio State University Wexner Medical Center, Columbus, Ohio.
Sarah E PanzerDepartment of Medicine, University of Wisconsin-Madison Hospital and Clinics, Madison, Wisconsin.
Weixiong ZhongDepartment of Medicine, University of Wisconsin-Madison Hospital and Clinics, Madison, Wisconsin.
Paolo CravediDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Chiara CantarelliDipartimento di Medicina e Chirurgia, Università di Parma, UO Nefrologia, Azienda Ospedaliero-Universitaria di Parma, Parma, Italy.
Liudmila KulikDepartment of Medicine, Anschutz Medical Campus, University of Colorado School of Medicine, Aurora, Colorado.
Zhiying YouDepartment of Medicine, Anschutz Medical Campus, University of Colorado School of Medicine, Aurora, Colorado.
Simon SatchellBristol Renal, Faculty of Health Sciences, University of Bristol, Bristol, United Kingdom.
Brad RovinDepartment of Internal Medicine, Ohio State University Wexner Medical Center, Columbus, Ohio.
Fei LiuQ32 Bio, Incorporated, Cambridge, Massachusetts.
Susan L KalledQ32 Bio, Incorporated, Cambridge, Massachusetts.
V Michael HolersDepartment of Medicine, Anschutz Medical Campus, University of Colorado School of Medicine, Aurora, Colorado.
Diana JalalDepartment of Medicine, University of Iowa Hospitals and Clinics, Iowa City, Iowa.
Joshua M ThurmanDepartment of Medicine, Anschutz Medical Campus, University of Colorado School of Medicine, Aurora, Colorado.ORCID 0000-0001-9062-3559
University of Colorado Anschutz Medical Campus · USNYU Langone Health · USThe Ohio State University Wexner Medical Center · USUniversity of Wisconsin–Madison · USIcahn School of Medicine at Mount Sinai · USOspedale di Parma · ITUniversity of Bristol · GBUniversity of Iowa Hospitals and Clinics · US

Funding

Training Program in Clinical & Translationa Research in Human Glomerular DiseaseU54DK083912 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GIPSON, DEBBIE S · 2009 to 2023
$20.3M
The Complement System and Ischemic Acute Renal FailureR01DK076690 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Joshua M Thurman · 2008 to 2026
$6.6M
Immunologic Mechanisms of Progressive GlomerulosclerosisR01DK113586 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI THURMAN, JOSHUA M · 2017 to 2020
$1.4M
Improving long-term allograft survival in kidney transplantation by targeting B cell survival cytokinesK23DK122136 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI PANZER, SARAH E · 2019 to 2022
$663k
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) DK076690HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) DK113586NIDDK NIH HHS K23 DK122136NIDDK NIH HHS R01 DK076690NIDDK NIH HHS R01 DK113586NIDDK NIH HHS U54 DK083912
6 · The paper itself

Abstract

Focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) are common forms of idiopathic nephrotic syndrome. The causes of these diseases are incompletely understood, but the response of patients to immunosuppressive therapies suggests that their pathogenesis is at least in part immune mediated. Preclinical and clinical research indicates that activation of the classical pathway of complement contributes to glomerular injury in FSGS. Glomerular IgM deposits are also prominent in some patients, raising the possibility that IgM is a trigger of classical pathway activation. In the present study, we examined the pattern of complement activation in the glomeruli and plasma of patients with nephrotic syndrome. We also tested whether patients with FSGS and MCD have elevated levels of natural IgM reactive with epitopes on glomerular endothelial cells and cardiolipin. We found evidence of classical pathway activation in patients with idiopathic nephrotic syndrome compared with healthy control subjects. We also detected higher levels of self-reactive IgM to both targets. Based on these results, IgM and classical pathway activation may contribute to disease pathogenesis in some patients with FSGS and MCD.

Indexed as

Complement Pathway, ClassicalEpitopesAdultAgedAntibody SpecificityCardiolipinsCase-Control StudiesComplement System ProteinsEndothelial CellsFemaleGlomerulosclerosis, Focal SegmentalHumansImmunoglobulin MImmunosuppressive AgentsKidney GlomerulusMaleCardiolipinsComplement System ProteinsEpitopesImmunoglobulin MImmunosuppressive Agentscomplementfocal segmental glomerulosclerosisIgMminimal change diseasenephrotic syndrome

Identifiers

PMID34459222
PMCPMC8560405
OpenAlexW3197065228

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.