Evidence map›Paper›PMID 26445497›Full record

ArticlePloS one2015

Toll-Like Receptor Family Polymorphisms Are Associated with Primary Renal Diseases but Not with Renal Outcomes Following Kidney Transplantation.

Mark C Dessing, Jesper Kers, Jeffrey Damman, Henri G D Leuvenink, Harry van Goor, Jan-Luuk Hillebrands, Bouke G Hepkema, Harold Snieder, Jacob van den Born, Martin H de Borst and 6 more

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

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

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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

16 authors at 6 institutions in 3 countries.

Mark C DessingDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands; Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, California, United States of America.
Jesper KersDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Jeffrey DammanDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Henri G D LeuveninkDepartment of Surgery, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Harry van GoorDepartment of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Jan-Luuk HillebrandsDepartment of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Bouke G HepkemaDepartment of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Harold SniederDepartment of Epidemiology, Unit of Genetic Epidemiology & Bioinformatics, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Jacob van den BornDepartment of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Martin H de BorstDepartment of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Stephan J L BakkerDepartment of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Gerjan J NavisDepartment of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Rutger J PloegNuffield Department of Surgical Sciences, University of Oxford, Oxford, United Kingdom.
Sandrine FlorquinDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands; Department of Pathology, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands.
Marc SeelenDepartment of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Jaklien C LeemansDepartment of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
University Medical Center Groningen · NLUniversity of Groningen · NLUniversity of Amsterdam · NLAcademic Medical Center · NLRadboud University Nijmegen · NLUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors (TLRs) play a crucial role in innate- and adaptive immunity. The TLR pathways were shown to play key functional roles in experimental acute and chronic kidney injury, including the allo-immune response after experimental renal transplantation. Data about the precise impact of TLRs and their negative regulators on human renal transplant outcomes however are limited and contradictory. We studied twelve non-synonymous single nucleotide polymorphisms (SNPs) of which eleven in TLR1-8 and one in SIGIRR in a final cohort comprising 1116 matching donors and recipients. TLR3 p.Leu412Phe and SIGIRR p.Gln312Arg significantly deviated from Hardy-Weinberg equilibrium and were excluded. The frequency distribution of the minor alleles of the remaining 10 TLR variants were compared between patients with end-stage renal disease (recipients) and controls (kidney donors) in a case-control study. Secondly, the associations between the minor allele frequency of the TLR variants and delayed graft function, biopsy-proven acute rejection and death-censored graft failure after transplantation were investigated with Cox regression. Carrier frequencies of the minor alleles of TLR1 p.His305Leu (OR = 4.79, 95% CI = 2.35-9.75, P = 0.0002), TLR1 p.Asn248Ser (OR = 1.26, 95% CI = 1.07-1.47, P = 0.04) and TLR8 p.Met1Val (OR = 1.37, 95% CI = 1.14-1.64, P = 0.008) were significantly higher in patients with ESRD, with little specificity for the underlying renal disease entity (adjusted for age, gender and donor-recipient relatedness). The minor allele frequency of none of the TLR variants significantly associated with the surrogate and definite outcomes, even when multivariable models were created that could account for TLR gene redundancy. In conclusion, genetic variants in TLR genes were associated with the prevalence of ESRD but not renal transplant outcomes. Therefore, our data suggests that specific TLR signaling routes might play a role in the final common pathway of primary renal injury. A role for TLR signaling in the context of renal transplantation is probably limited.

Indexed as

Kidney TransplantationPolymorphism, Single NucleotideAdultCase-Control StudiesDelayed Graft FunctionFemaleGene FrequencyGraft RejectionHumansKidney Failure, ChronicMaleMiddle AgedToll-Like ReceptorsTreatment OutcomeToll-Like Receptors

Identifiers

PMID26445497
PMCPMC4596574
OpenAlexW2305164061

What OpenQuestion holds

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Registered trials

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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.