Evidence map›Paper›PMID 33362783›Full record

ReviewFrontiers in immunology2020

Treatment of Rare Inflammatory Kidney Diseases: Drugs Targeting the Terminal Complement Pathway.

Marion Anliker-Ort, Jasper Dingemanse, John van den Anker, Priska Kaufmann

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Regulation of calcium homeostasis by S100A12 drives NETosis in chronic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  14. Kidney diseases.Immunological reviews · 2023
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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

4 authors at 3 institutions in 2 countries.

Marion Anliker-OrtDepartment of Clinical Pharmacology, Idorsia Pharmaceuticals Ltd, Allschwil, Switzerland.
Jasper DingemanseDepartment of Clinical Pharmacology, Idorsia Pharmaceuticals Ltd, Allschwil, Switzerland.
John van den AnkerPediatric Pharmacology and Pharmacometrics, University Children's Hospital Basel (UKBB), University of Basel, Basel, Switzerland.
Priska KaufmannDepartment of Clinical Pharmacology, Idorsia Pharmaceuticals Ltd, Allschwil, Switzerland.
Idorsia (Switzerland) · CHChildren's National · USUniversity Children’s Hospital Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complement system comprises the frontline of the innate immune system. Triggered by pathogenic surface patterns in different pathways, the cascade concludes with the formation of a membrane attack complex (MAC; complement components C5b to C9) and C5a, a potent anaphylatoxin that elicits various inflammatory signals through binding to C5a receptor 1 (C5aR1). Despite its important role in pathogen elimination, priming and recruitment of myeloid cells from the immune system, as well as crosstalk with other physiological systems, inadvertent activation of the complement system can result in self-attack and overreaction in autoinflammatory diseases. Consequently, it constitutes an interesting target for specialized therapies. The paradigm of safe and efficacious terminal complement pathway inhibition has been demonstrated by the approval of eculizumab in paroxysmal nocturnal hematuria. In addition, complement contribution in rare kidney diseases, such as lupus nephritis, IgA nephropathy, atypical hemolytic uremic syndrome, C3 glomerulopathy, or antineutrophil cytoplasmic antibody-associated vasculitis has been demonstrated. This review summarizes the involvement of the terminal effector agents of the complement system in these diseases and provides an overview of inhibitors for complement components C5, C5a, C5aR1, and MAC that are currently in clinical development. Furthermore, a link between increased complement activity and lung damage in severe COVID-19 patients is discussed and the potential for use of complement inhibitors in COVID-19 is presented.

Indexed as

Antibodies, Monoclonal, HumanizedAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisComplement ActivationComplement C5aComplement Inactivating AgentsComplement Membrane Attack ComplexComplement System ProteinsGlomerulonephritis, IGAHumansKidneyKidney DiseasesLupus NephritisReceptor, Anaphylatoxin C5aAntibodies, Monoclonal, HumanizedC5AR1 protein, humanComplement C5aComplement Inactivating AgentsComplement Membrane Attack ComplexComplement System ProteinseculizumabReceptor, Anaphylatoxin C5aaHUSANCA-associated vasculitisC3 glomerulopathyC5 antagonistC5aR1 antagonistcomplement systemIgA nephropathylupus nephritis

Identifiers

PMID33362783
PMCPMC7758461
OpenAlexW3111780294

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.