Evidence map›Paper›PMID 24698514›Full record

Trial reportAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2014

Evaluation of molecular profiles in calcineurin inhibitor toxicity post-kidney transplant: input to chronic allograft dysfunction.

D G Maluf, C I Dumur, J L Suh, J K Lee, E P Cathro, A L King, L Gallon, K L Brayman, V R Mas

Open access · bronzeAbstract readComparative StudyRandomized Controlled Trial
In one paragraph

Trial report in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

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  16. Predictability of human differential gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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

9 authors at 3 institutions in 1 country.

D G Maluf *University of Virginia, Department of Surgery PO Box 800679, Charlottesville, VA 22908-0679.
C I Dumur *University of Virginia, Department of Pathology PO Box 800904, VA 22908-0214.
J L SuhUniversity of Virginia, Department of Surgery PO Box 800679, Charlottesville, VA 22908-0679.
J K LeeUniversity of Virginia, Division of Biostatistics PO Box 800717, VA 22298-0717.
E P CathroUniversity of Virginia, Department of Pathology PO Box 800904, VA 22908-0214.
A L KingVirginia Commonwealth University, Division of Nephrology PO Box 980662, VA 23298-0662.
L GallonNorthwestern University, Division of Nephrology, Department of Internal Medicine, Comprehensive Transplant Center Chicago, IL 60611.
K L BraymanUniversity of Virginia, Department of Surgery PO Box 800679, Charlottesville, VA 22908-0679.
V R MasUniversity of Virginia, Department of Surgery PO Box 800679, Charlottesville, VA 22908-0679.
University of Virginia · USVirginia Commonwealth University · USNorthwestern University · US

Funding

Molecular pathways leading to chronic graft dysfunctionR01DK080074 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI MAS, VALERIA RAQUEL · 2008 to 2012
$1.8M
Molecular biomarkers associated with calcineurin inhibitor mediated kidney injuryR21DK100678 · NIDDK · UNIVERSITY OF VIRGINIA · PI MALUF, DANIEL GERMAN · 2014 to 2015
$435k
NIDDK NIH HHS R01 DK080074NIDDK NIH HHS R01DK080074NIDDK NIH HHS R21 DK100678
6 · The paper itself

Abstract

The molecular basis of calcineurin inhibitor toxicity (CNIT) in kidney transplantation (KT) and its contribution to chronic allograft dysfunction (CAD) with interstitial fibrosis (IF) and tubular atrophy (TA) were evaluated by: (1) identifying specific CNIT molecular pathways that associate with allograft injury (cross-sectional study) and (2) assessing the contribution of the identified CNIT signature in the progression to CAD with IF/TA (longitudinal study). Kidney biopsies from well-selected transplant recipients with histological diagnosis of CNIT (n = 14), acute rejection (n = 13) and CAD with IF/TA (n = 10) were evaluated. Normal allografts (n = 18) were used as controls. To test CNIT contribution to CAD progression, an independent set of biopsies (n = 122) from 61 KT patients collected at 3 and ~12 months post-KT (range = 9-18) were evaluated. Patients were classified based on 2-year post-KT graft function and histological findings as progressors (n = 30) or nonprogressors to CAD (n = 31). Molecular signatures characterizing CNIT samples were identified. Patients classified as progressors showed an overlap of 7% and 22% with the CNIT signature at 3 and at ~12 months post-KT, respectively, while the overlap was <1% and 1% in nonprogressor patients, showing CNIT at the molecular level as a nonimmunological factor involved in the progression to CAD.

Indexed as

Gene Expression ProfilingKidney TransplantationAdultAllograftsArea Under CurveBiomarkersCalcineurin InhibitorsCross-Sectional StudiesDisease ProgressionFemaleFollow-Up StudiesGraft RejectionHumansKidney Failure, ChronicLongitudinal StudiesMaleBiomarkersCalcineurin InhibitorsBiomarkerscalcineurin inhibitorskidney transplanttoxicity

Identifiers

PMID24698514
PMCPMC4377109
OpenAlexW1899618550

What OpenQuestion holds

Textmetadata
LicenceTDM
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.