Evidence map›Paper›PMID 27325183›Full record

ReviewKidney international2016

Targeting the complement cascade: novel treatments coming down the pike.

Joshua M Thurman, Moglie Le Quintrec

Open access · bronzeAbstract readReview
In one paragraph

Review in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.4field-weighted citation impact, top 7% 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, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The complement system in pediatric acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2023
    Review
  5. Article
  6. Review
  7. The role of C5a-C5aR1 axis in bone pathophysiology: A mini-review.Frontiers in cell and developmental biology · 2022
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Complement and the Kidney: An Overview.Advances in chronic kidney disease · 2020
    Review
  14. Review
  15. Review
  16. Complement and Complement Targeting Therapies in Glomerular Diseases.International journal of molecular sciences · 2019
    Review
  17. Review
  18. Review
  19. Role of Complement Activation in Allograft Inflammation.Current transplantation reports · 2019
    Article
  20. Review
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 2 institutions in 2 countries.

Joshua M ThurmanDepartment of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA. Electronic address: Joshua.Thurman@ucdenver.edu.
Moglie Le QuintrecDepartment of Nephrology and Renal Transplantation, Lapeyronnie Hospital and INSERM U1183, Institute of Regenerative Medicine and Biotherapies, Montpellier, France.
Inserm · FRUniversity of Colorado Anschutz Medical Campus · US

Funding

The Complement System and Ischemic Acute Renal FailureR01DK076690 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Joshua M Thurman · 2008 to 2026
$6.6M
NIDDK NIH HHS R01 DK076690
6 · The paper itself

Abstract

The complement cascade is a vital component of both the innate and adaptive immune systems. Complement activation also contributes to the pathogenesis of many diseases, however, and the kidney is particularly susceptible to complement-mediated injury. Drugs that block complement activation can rapidly reduce tissue inflammation and also attenuate the adaptive immune response to foreign and tissue antigens. Eculizumab is a monoclonal antibody that prevents the cleavage of C5. It has been approved for the treatment of atypical hemolytic uremic syndrome, and it has been used in selected patients with other kidney diseases. Many additional drugs are also in development for blocking the complement cascade, including new monoclonal antibodies, recombinant proteins, small molecules, and small interfering RNA agents. Validation of these new drugs as effective treatments for kidney diseases faces several challenges. Many complement-mediated kidney diseases are rare, so it is not feasible to test all of the new drugs in numerous different rare diseases. The onset and course of the diseases are heterogeneous; many of these diseases also carry a lifelong risk of recurrence, and it is not clear how long complement inhibition must be maintained. In spite of these challenges, new therapeutic options for targeting the complement system will likely become available in the near future and may prove useful for treating patients with kidney disease.

Indexed as

Adaptive ImmunityAntibodies, Monoclonal, HumanizedChoroiditisComplement ActivationComplement Inactivating AgentsComplement System ProteinsHumansImmunity, InnateKidneyKidney DiseasesMultifocal ChoroiditisRecurrenceAntibodies, Monoclonal, HumanizedComplement Inactivating AgentsComplement System Proteinseculizumabcomplementglomerulonephritisinflammation

Identifiers

PMID27325183
PMCPMC5026560
OpenAlexW2438363457

What OpenQuestion holds

Textmetadata
LicenceTDM
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.