Evidence map›Paper›PMID 25833956›Full record

Trial reportBlood2015

Eculizumab reduces complement activation, inflammation, endothelial damage, thrombosis, and renal injury markers in aHUS.

Roxanne Cofiell, Anjli Kukreja, Krystin Bedard, Yan Yan, Angela P Mickle, Masayo Ogawa, Camille L Bedrosian, Susan J Faas

2 registry-linked trialsOpen access · bronzeAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 108 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 3 pooled it
9.8field-weighted citation impact, top 1% 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.

NCT01194973 phase2completednot on this map

An Open-label, Multi-center Clinical Trial of Eculizumab in Adult Patients With Atypical Hemolytic-uremic Syndrome

TypeinterventionalSponsorAlexion Pharmaceuticals, Inc.Ran2010 to 2014Enrolled44ConditionsAtypical Hemolytic-Uremic SyndromeArmsEculizumab
NCT05684159 phase2not yet recruitingnot on this mapstarted 2027, after this paper: background citation

A Phase II, Open-Label Study of NM8074 in Patients With Atypical Hemolytic Uremic Syndrome (aHUS)

TypeinterventionalSponsorNovelMed TherapeuticsRan2027 to 2031Enrolled12ConditionsaHUS - Atypical Hemolytic Uremic SyndromeArmsNM8074
3 · Its place in the literature

Who cites it

108 citing papers in PubMed, 3 syntheses or guidelines pooled it, 195 citations in OpenAlex.

  1. Systematic review of atypical hemolytic uremic syndrome biomarkers.Pediatric nephrology (Berlin, Germany) · 2022
    Pooled it
  2. Interventions for atypical haemolytic uraemic syndrome.The Cochrane database of systematic reviews · 2021
    Pooled it
  3. Guideline
  4. Trial
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. A Web of Challenges: The Therapeutic Struggle to Target NETs in Disease.International journal of molecular sciences · 2025
    Review
  20. Review

48 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 1 country.

Roxanne CofiellAlexion Pharmaceuticals, Inc., Cheshire, CT.
Anjli KukrejaAlexion Pharmaceuticals, Inc., Cheshire, CT.
Krystin BedardAlexion Pharmaceuticals, Inc., Cheshire, CT.
Yan YanAlexion Pharmaceuticals, Inc., Cheshire, CT.
Angela P MickleAlexion Pharmaceuticals, Inc., Cheshire, CT.
Masayo OgawaAlexion Pharmaceuticals, Inc., Cheshire, CT.
Camille L BedrosianAlexion Pharmaceuticals, Inc., Cheshire, CT.
Susan J FaasAlexion Pharmaceuticals, Inc., Cheshire, CT.
Alexion Pharmaceuticals (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atypical hemolytic uremic syndrome (aHUS) is a genetic, life-threatening disease characterized by uncontrolled complement activation, systemic thrombotic microangiopathy (TMA), and vital organ damage. We evaluated the effect of terminal complement blockade with the anti-C5 monoclonal antibody eculizumab on biomarkers of cellular processes involved in TMA in patients with aHUS longitudinally, during up to 1 year of treatment, compared with in healthy volunteers. Biomarker levels were elevated at baseline in most patients, regardless of mutational status, plasma exchange/infusion use, platelet count, or lactate dehydrogenase or haptoglobin levels. Eculizumab reduced terminal complement activation (C5a and sC5b-9) and renal injury markers (clusterin, cystatin-C, β2-microglobulin, and liver fatty acid binding protein-1) to healthy volunteer levels and reduced inflammation (soluble tumor necrosis factor receptor-1), coagulation (prothrombin fragment F1+2 and d-dimer), and endothelial damage (thrombomodulin) markers to near-normal levels. Alternative pathway activation (Ba) and endothelial activation markers (soluble vascular cell adhesion molecule-1) decreased but remained elevated, reflecting ongoing complement activation in aHUS despite complete terminal complement blockade. These results highlight links between terminal complement activation and inflammation, endothelial damage, thrombosis, and renal injury and underscore ongoing risk for systemic TMA and progression to organ damage. Further research regarding underlying complement dysregulation is warranted. This trial was registered at www.clinicaltrials.gov as #NCT01194973.

Indexed as

Acute Kidney InjuryAdultAntibodies, Monoclonal, HumanizedAtypical Hemolytic Uremic SyndromeBiomarkersComplement ActivationEndothelium, VascularFemaleHumansInflammationMaleThrombosisAntibodies, Monoclonal, HumanizedBiomarkerseculizumab

Identifiers

PMID25833956
PMCPMC4449039
OpenAlexW2040109924

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.