Evidence map›Paper›PMID 34220921›Full record

ArticleFrontiers in genetics2021

Case Report: A Rare Truncating Variant of the

Gabriella Guzzo, Salima Sadallah, Heidi Fodstad, Jean-Pierre Venetz, Samuel Rotman, Daniel Teta, Thierry Gauthier, Giuseppe Pantaleo, Andrea Superti-Furga, Manuel Pascual

Open access · goldAbstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

10 authors at 3 institutions in 1 country.

Gabriella GuzzoOrgan Transplant Center, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Salima SadallahService of Immunology and Allergy, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Heidi FodstadDivision of Genetic Medicine, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Jean-Pierre VenetzOrgan Transplant Center, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Samuel RotmanService of Clinical Pathology, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Daniel TetaService of Nephrology, Valais Hospital, Sion, Switzerland.
Thierry GauthierHôpital Riviera Chablais, Vevey, Switzerland.
Giuseppe PantaleoService of Immunology and Allergy, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Andrea Superti-FurgaDivision of Genetic Medicine, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Manuel PascualOrgan Transplant Center, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
University of Lausanne · CHHôpital du Valais · CHHôpital Riviera-Chablais · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Despite appropriate therapy, 20-40% of affected-patients evolve toward end-stage kidney disease (ESKD). Mesangial IgA deposits are the hallmark of IgAN, and complement deposition (C3) seems to differentiate latent IgA mesangial deposits from active IgAN. Atypical hemolytic uremic syndrome (aHUS), another disease in which complement plays an important role, is caused by inherited or acquired deregulation of the alternative pathway (AP) of complement. A subgroup of IgAN shows thrombotic microangiopathy (TMA) lesions in kidney biopsies, the histological characteristic of aHUS. Genetic variants of complement Factor H (CFH), known to be present in aHUS, have been associated with rapidly progressive forms of IgAN and a clinical pattern of aHUS. Genome-wide association studies (GWAS) have confirmed that the 1q32 region, encoding for

Indexed as

atypical hemolytic uremic syndromeCFHCFHR5complementeculizumabIgA nephropathythrombotic microangiopathy (TA-TMA)

Identifiers

PMID34220921
PMCPMC8244589
OpenAlexW3164771321

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.