Evidence map›Paper›PMID 38578365›Full record

ReviewPathologie (Heidelberg, Germany)2024

[The complement cascade in renal pathology].

E Vonbrunn, C Daniel

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pathologie (Heidelberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

2 authors at 1 institution in 1 country.

E VonbrunnAbteilung Nephropathologie, Pathologisches Institut, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Krankenhausstr. 8-10, 91054, Erlangen, Deutschland.
C DanielAbteilung Nephropathologie, Pathologisches Institut, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Krankenhausstr. 8-10, 91054, Erlangen, Deutschland. Christoph.Daniel@uk-erlangen.de.ORCID http://orcid.org/0000-0002-6803-4755
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

Deutsche Forschungsgemeinschaft (DFG) 509149993
6 · The paper itself

Abstract

The complement cascade comprises a variety of soluble and cell surface proteins and is an important component of the innate immune system. When the cascade is triggered by any of the three activation pathways, the complement system rapidly produces large amounts of protein fragments that are potent mediators of inflammatory, vasoactive, and metabolic responses. All activation pathways lead to the terminal complement cascade with the formation of the membrane attack complex, which lyses cells by forming membrane pores. Although the complement system is essential for pathogen defense and homeostasis, excessive or uncontrolled activation can lead to tissue damage. Recent research shows that the complement system is activated in almost all kidney diseases, even those not traditionally considered immune-mediated. In directly complement-mediated kidney diseases, complement factors or regulators are defective, afunctional or inactivated by antibodies. In many other renal diseases, the complement system is activated secondarily as a result of renal damage and is therefore involved in the pathogenesis of the disease, but is not the trigger. The detection of complement deposits is also used to diagnose kidney disease. This review describes the structure of the complement system and the effects of its dysregulation as a cause and modulator of renal disease.

Indexed as

Complement ActivationComplement System ProteinsKidney DiseasesComplement Membrane Attack ComplexHumansImmunity, InnateKidneyComplement Membrane Attack ComplexComplement System ProteinsAntibodiesC3GImmune systemLectinMicroangiopathy

Identifiers

PMID38578365
OpenAlexW4393994053

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.