Evidence map›Paper›PMID 25956757›Full record

ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2015

Urine podocyte mRNAs mark disease activity in IgA nephropathy.

Akihiro Fukuda, Yuji Sato, Takashi Iwakiri, Hiroyuki Komatsu, Masao Kikuchi, Kazuo Kitamura, Roger C Wiggins, Shouichi Fujimoto

Open access · bronzeAbstract read
In one paragraph

Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 34 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

8 authors at 2 institutions in 2 countries.

Akihiro FukudaFirst Department of Internal Medicine, University of Miyazaki, Miyazaki, Japan.
Yuji SatoFirst Department of Internal Medicine, University of Miyazaki, Miyazaki, Japan.
Takashi IwakiriFirst Department of Internal Medicine, University of Miyazaki, Miyazaki, Japan.
Hiroyuki KomatsuFirst Department of Internal Medicine, University of Miyazaki, Miyazaki, Japan.
Masao KikuchiFirst Department of Internal Medicine, University of Miyazaki, Miyazaki, Japan.
Kazuo KitamuraFirst Department of Internal Medicine, University of Miyazaki, Miyazaki, Japan.
Roger C WigginsDivision of Nephrology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Shouichi FujimotoFirst Department of Internal Medicine, University of Miyazaki, Miyazaki, Japan Department of Hemovascular Medicine and Artificial Organs, University of Miyazaki, Miyazaki, Japan.
University of Miyazaki · JPUniversity of Michigan–Ann Arbor · US

Funding

The Glomerular PodocyteR01DK046073 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WIGGINS, ROGER CHARLES · 1993 to 2015
$4.7M
NIDDK NIH HHS R01 DK046073PHS HHS DKR0146073
6 · The paper itself

Abstract

backgroundPodocyte depletion is a major mechanism driving glomerulosclerosis. We and others have previously projected from model systems that podocyte-specific mRNAs in the urine pellet might serve as glomerular disease markers. We evaluated IgA nephropathy (IgAN) to test this concept.

methodsFrom 2009 to 2013, early morning voided urine samples and kidney biopsies from IgAN patients (n = 67) were evaluated in comparison with urine samples from healthy age-matched volunteers (n = 28). Urine podocyte (podocin) mRNA expressed in relation to either urine creatinine concentration or a kidney tubular marker (aquaporin 2) was tested as markers.

resultsUrine podocyte mRNAs were correlated with the severity of active glomerular lesions (segmental glomerulosclerosis and acute extracapillary proliferation), but not with non-glomerular lesions (tubular atrophy/interstitial fibrosis) or with clinical parameters of kidney injury (serum creatinine and estimated glomerular filtration rate), or with degree of accumulated podocyte loss at the time of biopsy. In contrast, proteinuria correlated with all histological and clinical markers. Glomerular tuft podocyte nuclear density (a measure of cumulative podocyte loss) correlated with tubular atrophy/interstitial fibrosis, estimated-glomerular filtration rate and proteinuria, but not with urine podocyte markers. In a subset of the IgA cohort (n = 19, median follow-up period = 37 months), urine podocyte mRNAs were significantly decreased after treatment, in contrast to proteinuria which was not significantly changed.

conclusionsUrine podocyte mRNAs reflect active glomerular injury at a given point in time, and therefore provide both different and additional clinical information that can complement proteinuria in the IgAN decision-making paradigm.

Indexed as

AdultBiomarkersCells, CulturedFemaleGlomerular Filtration RateGlomerulonephritis, IGAHumansKidney GlomerulusMalePodocytesPrognosisProteinuriaReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerBiomarkersRNA, Messengerglomerular diseaseIgA nephropathypodocyteproteinuriaurine podocyte mRNA

Identifiers

PMID25956757
PMCPMC4479668
OpenAlexW1925836265

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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.