Evidence map›Paper›PMID 30910380›Full record

ArticleKidney international2019

Differential contribution of C5aR and C5b-9 pathways to renal thrombic microangiopathy and macrovascular thrombosis in mice carrying an atypical hemolytic syndrome-related factor H mutation.

Yoshiyasu Ueda, Takashi Miwa, Daisuke Ito, Hangsoo Kim, Sayaka Sato, Damodar Gullipalli, Lin Zhou, Madhu Golla, Delu Song, Joshua L Dunaief and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2019. 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
2.0field-weighted citation impact, top 13% 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, 39 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Yoshiyasu UedaDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Takashi MiwaDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Daisuke ItoDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Hangsoo KimDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Sayaka SatoDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Damodar GullipalliDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Lin ZhouDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Madhu GollaDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Delu SongDepartment of Ophthalmology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Joshua L DunaiefDepartment of Ophthalmology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Matthew B PalmerDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Wen-Chao SongDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Electronic address: songwe@pennmedicine.upenn.edu.
University of Pennsylvania · USTranslational Therapeutics (United States) · US

Funding

BIOLOGY OF DECAY ACCELERATING FACTORR01AI044970 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SONG, WENCHAO · 2000 to 2014
$4.9M
Pathogenesis and therapy of dense deposit disease in a mouse modelR01AI085596 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SONG, WENCHAO · 2010 to 2019
$3.5M
Complement dysregulation and atypical hemolytic uremic syndromeR01AI117410 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SONG, WENCHAO · 2015 to 2019
$2.0M
Membrane complement regulators in RPE degeneration and retinal injuryR01EY023709 · NEI · UNIVERSITY OF PENNSYLVANIA · PI SONG, WENCHAO · 2013 to 2016
$2.0M
NEI NIH HHS R01 EY023709NIAID NIH HHS R01 AI044970NIAID NIH HHS R01 AI085596NIAID NIH HHS R01 AI117410
6 · The paper itself

Abstract

Atypical hemolytic uremic syndrome (aHUS) is a form of thrombotic microangiopathy (TMA) caused by dysregulated complement activation. Clinically, aHUS is effectively treated by an anti-C5 monoclonal antibody (mAb) but whether the disease is mediated by the C5a receptor (C5aR) or C5b-9 pathway, or both, is unknown. Here we address this in a factor H mutant mouse (FH

Indexed as

AnimalsAntibodies, MonoclonalAtypical Hemolytic Uremic SyndromeComplement ActivationComplement C6Complement Factor HComplement Membrane Attack ComplexDisease Models, AnimalFemaleHumansKidney GlomerulusMaleMiceMice, TransgenicMicroscopy, ElectronPoint MutationAntibodies, MonoclonalC5ar1 protein, mouseComplement C6Complement Factor HComplement Membrane Attack ComplexReceptor, Anaphylatoxin C5aatypical hemolytic uremic syndromeC5a receptorcomplementmembrane attack complexthrombotic microangiopathy

Identifiers

PMID30910380
PMCPMC10084839
OpenAlexW2916939869

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.