Evidence map›Paper›PMID 34613485›Full record

ReviewCell and tissue research2021

Complement catalyzing glomerular diseases.

Peter F Zipfel, Thorsten Wiech, Hermann-Josef Gröne, Christine Skerka

Abstract readReview
In one paragraph

Review in Cell and tissue research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. The Src-Family Kinases Hck, Fgr and Lyn Drive Immune Complex-Mediated Glomerulonephritis Through the Syk Tyrosine Kinase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Functional variant rs12614 inFrontiers in immunology · 2022
    Article
  17. Article
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

4 authors.

Peter F ZipfelDepartment of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, Jena, Germany. peter.zipfel@leibniz-jena.de.ORCID http://orcid.org/0000-0002-6149-2411
Thorsten WiechInstitute of Pathology, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
Hermann-Josef GröneInstitute of Pathology, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
Christine SkerkaDepartment of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, Jena, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement is an evolutionarily conserved system which is important in the defense against microorganisms and also in the elimination of modified or necrotic elements of the body. Complement is activated in a cascade type manner and activation and all steps of cascade progression are tightly controlled and regulatory interleaved with many processes of inflammatory machinery. Overshooting of the complement system due to dysregulation can result in the two prototypes of primary complement mediated renal diseases: C3 glomerulopathy and thrombotic microangiopathy. Apart from these, complement also is highly activated in many other inflammatory native kidney diseases, such as membranous nephropathy, ANCA-associated necrotizing glomerulonephritis, and IgA nephropathy. Moreover, it likely plays an important role also in the transplant setting, such as in antibody-mediated rejection or in hematopoietic stem cell transplant associated thrombotic microangiopathy. In this review, these glomerular disorders are discussed with regard to the role of complement in their pathogenesis. The consequential, respective clinical trials for complement inhibitory therapy strategies for these diseases are described.

Indexed as

AnimalsHumansKidneyKidney GlomerulusC3 Convertase testingC3 glomerulopathyComplementComplement diagnosticsGlomerular diseasesThrombotic microangiopathy

Identifiers

PMID34613485
PMCPMC8523427

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.