Evidence map›Paper›PMID 35368114›Full record

ArticleClinical transplantation2022

IFNL4 rs368234815 polymorphism does not predict risk of BK virus associated nephropathy after living-donor kidney transplant: A case-control study.

Ursula Tanriver, Florian Emmerich, Jonas Florian Hummel, Bernd Jänigen, Marcus Panning, Frederic Arnold, Yakup Tanriver

Open access · hybridAbstract read
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In one paragraph

Article in Clinical transplantation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 56% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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

7 authors at 1 institution in 2 countries.

Ursula TanriverDepartment of Hematology and Oncology, University Children's Hospital Basel, University of Basel, Basel, Switzerland.ORCID 0000-0002-4573-8856
Florian EmmerichInstitute for Transfusion Medicine and Gene Therapy, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Jonas Florian HummelInstitute of Medical Microbiology and Hygiene, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Bernd JänigenDepartment of General and Digestive Surgery: Section of Transplant Surgery, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0000-0001-9401-8815
Marcus PanningInstitute of Virology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Frederic ArnoldInstitute of Medical Microbiology and Hygiene, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Yakup TanriverInstitute of Medical Microbiology and Hygiene, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0000-0002-4806-2548
University of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBK polyoma virus (BKPyV) associated nephropathy (BKPyVAN) is a major cause of kidney graft loss in renal transplant patients. Interferons (IFNs) are an important innate immune response against viral infections and genetic polymorphisms of the IFN-pathways can affect susceptibility and mortality during viral infection. Here, we investigated whether the dinucleotide polymorphism rs368234815 (ΔG/TT) in the IFNL4 gene contributed to BKPyV reactivation or BKPyVAN after living-donor kidney transplantation.

methodsThis retrospective case-control study determines the prevalence of IFNL4 variants in a Caucasian population of living-donor kidney transplant recipients and donors and explores its association with BKPyV infection and BKPyVAN development. We included 28 recipients with BKPyV reactivation, 10 of which developed BKPyVAN and 30 BKPyV negative controls. Targeted sequencing of the IFNL4 gene from both recipients and their respective donors was performed.

resultsWe found IFNL4 rs368234815 ΔG allele frequencies of 41.7% in BKPyV negative and 39.3% in BKPyV positive recipients (P = .85), and 41.7% and 40.4% (P>.99) in their respective donors. IFNL4 rs368234815 ΔG allele frequencies in BKPyVAN developing recipients and their respective donors were 50% and 43.7% (P = .60 and P>.99).

conclusionsOur results indicate that the IFNL4 rs368234815 ΔG allele is not associated with BKPyV reactivation, nor the manifestation of BKPyVAN.

Indexed as

BK VirusKidney TransplantationPolyomavirus InfectionsTumor Virus InfectionsCase-Control StudiesHumansInterferon LambdaInterleukinsLiving DonorsPolymorphism, GeneticRetrospective StudiesTransplant RecipientsIFNL4 protein, humanInterferon LambdaInterleukinsallograft rejectionBK virusIFNL4 polymorphismsliving-donor kidney transplantpolyomavirus associated nephropathy

Identifiers

PMID35368114
PMCPMC9539699
OpenAlexW4225622021

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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.