Evidence map›Paper›PMID 30794652›Full record

Trial reportPloS one2019

The association of HLA-G polymorphisms and the synergistic effect of sMICA and sHLA-G with chronic kidney disease and allograft acceptance.

Vanessa Hauer, Matilde Risti, Bruna L M Miranda, José S da Silva, Ana L Cidral, Carolina M Pozzi, Fabiana L de C Contieri, Ibrahim A Sadissou, Eduardo A Donadi, Danillo G Augusto and 1 more

Open access · goldAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 14 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

11 authors at 4 institutions in 1 country.

Vanessa HauerLaboratório de Imunogenética e Histocompatibilidade, Departamento de Genética, Universidade Federal do Paraná, Curitiba, Paraná, Brazil.ORCID 0000-0002-3170-5383
Matilde RistiLaboratório de Imunogenética e Histocompatibilidade, Departamento de Genética, Universidade Federal do Paraná, Curitiba, Paraná, Brazil.ORCID 0000-0002-4841-3109
Bruna L M MirandaLaboratório de Imunogenética e Histocompatibilidade, Departamento de Genética, Universidade Federal do Paraná, Curitiba, Paraná, Brazil.
José S da SilvaLaboratório de Imunogenética e Histocompatibilidade, Departamento de Genética, Universidade Federal do Paraná, Curitiba, Paraná, Brazil.
Ana L CidralLaboratório de Imunogenética e Histocompatibilidade, Departamento de Genética, Universidade Federal do Paraná, Curitiba, Paraná, Brazil.ORCID 0000-0003-0839-1977
Carolina M PozziSetor de Transplante Renal, Hospital Universitário Evangélico de Curitiba, Alameda Augusto Stellfeld, Curitiba, Brazil.
Fabiana L de C ContieriSetor de Transplante Renal, Hospital Universitário Evangélico de Curitiba, Alameda Augusto Stellfeld, Curitiba, Brazil.
Ibrahim A SadissouLaboratório de Biologia Molecular, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo, Ribeirão Preto, São Paulo, Brazil.
Eduardo A DonadiLaboratório de Biologia Molecular, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo, Ribeirão Preto, São Paulo, Brazil.
Danillo G AugustoLaboratório de Genética Molecular Humana, Departamento de Genética, Universidade Federal do Paraná, Curitiba, Paraná, Brazil.
Maria da G BicalhoLaboratório de Imunogenética e Histocompatibilidade, Departamento de Genética, Universidade Federal do Paraná, Curitiba, Paraná, Brazil.ORCID 0000-0002-0588-6096
Universidade Federal do Paraná · BRHospital Universitário Evangélico de Curitiba · BRUniversidade de Ribeirão Preto · BRUniversidade Estadual de Santa Cruz · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The HLA-G and MICA genes are stimulated under inflammatory conditions and code for soluble (sMICA and sHLA-G) or membrane-bound molecules that exhibit immunomodulatory properties. It is still unclear whether they would have a synergistic or antagonistic effect on the immunomodulation of the inflammatory response, such as in chronic kidney disease (CKD), contributing to a better prognosis after the kidney transplantation. In this study, we went from genetic to plasma analysis, first evaluating the polymorphism of MICA, NKG2D and HLA-G in a cohort from Southern Brazil, subdivided in a control group of individuals (n = 75), patients with CKD (n = 94), and kidney-transplant (KT) patients (n = 64). MICA, NKG2D and HLA-G genotyping was performed by polymerase chain reaction with specific oligonucleotide probes, Taqman and Sanger sequencing, respectively. Levels of soluble forms of MICA and HLA-G were measured in plasma with ELISA. Case-control analysis showed that the individuals with haplotype HLA-G*01:01/UTR-4 have a lower susceptibility to develop chronic kidney disease (OR = 0.480; p = 0.032). Concerning the group of kidney-transplant patients, the HLA-G genotypes +3010 GC (rs1710) and +3142 GC (rs1063320) were associated with higher risk for allograft rejection (OR = 5.357; p = 0.013 and OR = 5.357, p = 0.013, respectively). Nevertheless, the genotype +3010 GG (OR = 0.136; p = 0.041) was associated with kidney allograft acceptance, suggesting that it is a protection factor for rejection. In addition, the phenotypic analysis revealed higher levels of sHLA-G (p = 0.003) and sMICA (p < 0.001) in plasma were associated with the development of CKD. For patients who were already under chronic pathological stress and underwent a kidney transplant, a high sMICA (p = 0.001) in pre-transplant proved to favor immunomodulation and allograft acceptance. Even so, the association of genetic factors with differential levels of soluble molecules were not evidenced, we displayed a synergistic effect of sMICA and sHLA-G in response to inflammation. This increase was observed in CKD patients, that when undergo transplantation, had this previous amount of immunoregulatory molecules as a positive factor for the allograft acceptance.

Indexed as

Kidney TransplantationPolymorphism, GeneticAdultAllograftsCase-Control StudiesFemaleGraft RejectionHistocompatibility Antigens Class IHLA-G AntigensHumansMaleMiddle AgedNK Cell Lectin-Like Receptor Subfamily KRenal Insufficiency, ChronicRisk FactorsHistocompatibility Antigens Class IHLA-G AntigensKLRK1 protein, humanMHC class I-related chain ANK Cell Lectin-Like Receptor Subfamily K

Identifiers

PMID30794652
PMCPMC6386361
OpenAlexW2917399107

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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.