Evidence map›Paper›PMID 27003899›Full record

ArticleHepatology international2016

Role of cytokine gene polymorphisms in acute and chronic kidney disease following liver transplantation.

Hideya Kamei, Yasuharu Onishi, Taro Nakamura, Masatoshi Ishigami, Nobuyuki Hamajima

Abstract read
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In one paragraph

Article in Hepatology international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 2 pooled it
0.4field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 2 syntheses or guidelines pooled it, 9 citations in OpenAlex.

  1. Association ofFrontiers in genetics · 2020
    Pooled it
  2. Pooled it
  3. The Influence of Diabetes Mellitus on the Risks of End-Stage Kidney Disease and Mortality After Liver Transplantation.Transplant international : official journal of the European Society for Organ Transplantation · 2022
    Article
  4. Article
  5. Article
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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

5 authors at 2 institutions in 1 country.

Hideya KameiDepartment of Transplantation Surgery, Nagoya University Hospital, 65 Tsurumai, Showa, Nagoya, 466-8550, Japan. kamei@med.nagoya-u.ac.jp.
Yasuharu OnishiDepartment of Transplantation Surgery, Nagoya University Hospital, 65 Tsurumai, Showa, Nagoya, 466-8550, Japan.
Taro NakamuraDepartment of Transplantation Surgery, Nagoya University Hospital, 65 Tsurumai, Showa, Nagoya, 466-8550, Japan.
Masatoshi IshigamiDepartment of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa, Nagoya, 466-8550, Japan.
Nobuyuki HamajimaDepartment of Preventive Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa, Nagoya, 466-8550, Japan.
Nagoya University Hospital · JPNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeDevelopment of renal dysfunction, including acute kidney injury (AKI) and chronic kidney disease (CKD), after liver transplantation (LT) remains a critical issue adversely affecting patient survival in both the short and long term. Previous reports have suggested that inflammatory and antiinflammatory cytokines and their functionally relevant gene polymorphisms may play critical roles in the development of AKI and CKD. However, the involvement of these cytokines and their gene polymorphisms in renal deterioration following LT remains unclear.

methodsWe examined 62 recipients who underwent LT at Nagoya University between 2004 and 2009 and who had survived for at least 1 year. The following gene polymorphisms in recipients were analyzed: tumor necrosis factor-A (TNFA) T-1031C, interleukin-2 (IL2) T-330G, IL10 C-819T, IL13 C-1111T, transforming growth factor-B (TGFB) T29C, and IL4 T-33C.

resultsThirteen patients (21 %) developed AKI within 4 weeks after LT. Of the investigated gene polymorphisms, the IL4 -33 T/T genotype was significantly associated with higher incidence of AKI compared with the other two genotypes [hazard ratio (HR) = 5.48, 95 % confidence interval (CI) 1.18-25.52, p = 0.03]. On the other hand, 16 patients (26 %) had developed CKD at median follow-up of 9.2 years after LT. We showed the lack of association between investigated gene polymorphisms in recipients and CKD development.

conclusionsThe IL4 -33 T/T genotype might be a risk factor for AKI in LT, and this might contribute to earlier withdrawal of immunosuppressive agents to minimize renal toxicity. In contrast, none of the investigated cytokine gene polymorphisms were associated with CKD.

Indexed as

Acute Kidney InjuryAdultFemaleGenetic Predisposition to DiseaseHumansInterleukin-10Interleukin-13Interleukin-2Interleukin-4Liver TransplantationMaleMiddle AgedPolymorphism, Single NucleotideProportional Hazards ModelsRenal Insufficiency, ChronicRetrospective StudiesIL10 protein, humanIL13 protein, humanIL2 protein, humanIL4 protein, humanInterleukin-10Interleukin-13Interleukin-2Interleukin-4TNF protein, humanTransforming Growth Factor betaTumor Necrosis Factor-alphaAcute kidney injuryChronic kidney diseaseCytokineGene polymorphismLiver transplantation

Identifiers

PMID27003899
OpenAlexW2307867702

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.