Evidence map›Paper›PMID 24489795›Full record

Trial reportPloS one2014

Urine microRNA as potential biomarkers of autosomal dominant polycystic kidney disease progression: description of miRNA profiles at baseline.

Iddo Z Ben-Dov, Ying-Cai Tan, Pavel Morozov, Patricia D Wilson, Hanna Rennert, Jon D Blumenfeld, Thomas Tuschl

Registry-linked trialOpen access · goldAbstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03901521 (Autosomal Dominant Polycystic Kidney Disease Somatic Mutation Biorepository), which is not on this map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
11.0field-weighted citation impact, top 1% 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.

NCT03901521 enrolling by invitationnot on this mapstarted 2018, after this paper: background citation

Autosomal Dominant Polycystic Kidney Disease Somatic Mutation Biorepository

Typeobservational_patient_registrySponsorWeill Medical College of Cornell UniversityRan2018 to 2028Enrolled100ConditionsAutosomal Dominant Polycystic Kidney Disease
3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
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  6. Extracellular vesicles as tools and targets in therapy for diseases.Signal transduction and targeted therapy · 2024
    Review
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  20. Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases.International journal of molecular sciences · 2020
    Review
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 5 institutions in 2 countries.

Iddo Z Ben-DovLaboratory of RNA Molecular Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, New York, United States of America.
Ying-Cai TanMolecular Pathology Laboratory, New York Presbyterian Hospital, Cornell University, New York, New York, United States of America ; Pathology and Laboratory Medicine, Weill Medical College, Cornell University, New York, New York, United States of America.
Pavel MorozovLaboratory of RNA Molecular Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, New York, United States of America.
Patricia D WilsonCentre for Nephrology, University College London Medical School, London, United Kingdom.
Hanna RennertMolecular Pathology Laboratory, New York Presbyterian Hospital, Cornell University, New York, New York, United States of America ; Pathology and Laboratory Medicine, Weill Medical College, Cornell University, New York, New York, United States of America.
Jon D BlumenfeldRogosin Institute, Weill Medical College of Cornell University, New York, New York, United States of America.
Thomas TuschlLaboratory of RNA Molecular Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, New York, United States of America.
Howard Hughes Medical Institute · USNewYork–Presbyterian Hospital · USRockefeller University · USThe Rogosin Institute · USUniversity College London · GB

Funding

TRANSFORMING TRANSLATIONAL SCIENCE AND EDUCATION TO BENEFIT HUMAN HEALTHUL1RR024143 · NCRR · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 2006 to 2011
$49.1M
Clinical utility of extracellular RNA as marker of kidney disease progressionUH2TR000933 · NCATS · ROCKEFELLER UNIVERSITY · PI SUTHANTHIRAN, MANIKKAM, TUSCHL, THOMAS · 2013 to 2014
$988k
NCATS NIH HHS UH2 TR000933NCATS NIH HHS UH2TR000933NCRR NIH HHS UL1 RR024143NCRR NIH HHS UL1RR024143
6 · The paper itself

Abstract

backgroundAutosomal dominant polycystic kidney disease (ADPKD) is clinically heterogenic. Biomarkers are needed to predict prognosis and guide management. We aimed to profile microRNA (miRNA) in ADPKD to gain molecular insight and evaluate biomarker potential.

methodsSmall-RNA libraries were generated from urine specimens of ADPKD patients (N = 20) and patients with chronic kidney disease of other etiologies (CKD, N = 20). In this report, we describe the miRNA profiles and baseline characteristics. For reference, we also examined the miRNA transcriptome in primary cultures of ADPKD cyst epithelia (N = 10), normal adult tubule (N = 8) and fetal tubule (N = 7) epithelia.

resultsIn primary cultures of ADPKD kidney cells, miRNA cistrons mir-143(2) (9.2-fold), let-7i(1) (2.3-fold) and mir-3619(1) (12.1-fold) were significantly elevated compared to normal tubule epithelia, whereas mir-1(4) members (19.7-fold), mir-133b(2) (21.1-fold) and mir-205(1) (3.0-fold) were downregulated (P<0.01). Expression of the dysregulated miRNA in fetal tubule epithelia resembled ADPKD better than normal adult cells, except let-7i, which was lower in fetal cells. In patient biofluid specimens, mir-143(2) members were 2.9-fold higher in urine cells from ADPKD compared to other CKD patients, while expression levels of mir-133b(2) (4.9-fold) and mir-1(4) (4.4-fold) were lower in ADPKD. We also noted increased abundance mir-223(1) (5.6-fold), mir-199a(3) (1.4-fold) and mir-199b(1) (1.8-fold) (P<0.01) in ADPKD urine cells. In ADPKD urine microvesicles, miR-1(2) (7.2-fold) and miR-133a(2) (11.8-fold) were less abundant compared to other CKD patients (P<0.01).

conclusionsWe found that in ADPKD urine specimens, miRNA previously implicated as kidney tumor suppressors (miR-1 and miR-133), as well as miRNA of presumed inflammatory and fibroblast cell origin (miR-223/miR-199), are dysregulated when compared to other CKD patients. Concordant with findings in the primary tubule epithelial cell model, this suggests roles for dysregulated miRNA in ADPKD pathogenesis and potential use as biomarkers. We intend to assess prognostic potential of miRNA in a followup analysis.

Indexed as

Epigenesis, GeneticAdultAgedBiomarkersDisease ProgressionFemaleFetusGene LibraryHigh-Throughput Nucleotide SequencingHumansKidney TubulesMaleMicroRNAsMiddle AgedPolycystic Kidney, Autosomal DominantPrimary Cell CultureBiomarkersMicroRNAs

Identifiers

PMID24489795
PMCPMC3906110
OpenAlexW2015846801

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Registered trials

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.