Evidence map›Paper›PMID 28028615›Full record

ArticlePediatric nephrology (Berlin, Germany)2017

Podocyte number and density changes during early human life.

Masao Kikuchi, Larysa Wickman, Raja Rabah, Roger C Wiggins

Open access · hybridAbstract read
In one paragraph

Article in Pediatric nephrology (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  14. Observational
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  19. FSGS as an Adaptive Response to Growth-Induced Podocyte Stress.Journal of the American Society of Nephrology : JASN · 2017
    Article
  20. Are podocytes motile?Pflugers Archiv : European journal of physiology · 2017
    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

4 authors at 1 institution in 2 countries.

Masao KikuchiDepartment of Internal Medicine, Nephrology Division, University of Michigan, 1570B MSRBII, 1150 W Medical Center Drive, Ann Arbor, MI, 48109-0676, USA.
Larysa WickmanDepartment of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI, USA.
Raja RabahDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
Roger C WigginsDepartment of Internal Medicine, Nephrology Division, University of Michigan, 1570B MSRBII, 1150 W Medical Center Drive, Ann Arbor, MI, 48109-0676, USA. rwiggins@umich.edu.
University of Michigan–Ann Arbor · US

Funding

Training Program in Clinical & Translationa Research in Human Glomerular DiseaseU54DK083912 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KRETZLER, MATTHIAS · 2009 to 2023
$20.3M
University of Michigan O'Brien Kidney Translational Core CenterP30DK081943 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BROSIUS, FRANK C · 2008 to 2022
$12.9M
Podocyte Markers in Human Glomerular DiseasesR01DK102643 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WIGGINS, ROGER CHARLES · 2015 to 2017
$698k
NIDDK NIH HHS P30 DK081943NIDDK NIH HHS R01 DK102643NIDDK NIH HHS U54 DK083912
6 · The paper itself

Abstract

backgroundPodocyte depletion, which drives progressive glomerulosclerosis in glomerular diseases, is caused by a reduction in podocyte number, size or function in the context of increasing glomerular volume.

methodsKidneys obtained at autopsy from premature and mature infants who died in the first year of life (n = 24) were used to measure podometric parameters for comparison with previously reported data from older kidneys.

resultsGlomerular volume increased 4.6-fold from 0.13 ± 0.07 μm

conclusionsAs glomeruli continue to enlarge, podocyte density (number per volume) rapidly decreases, requiring a parallel rapid increase in podocyte size that allows podocyte foot processes to maintain complete coverage of the filtration surface area. Hypertrophic stresses on the glomerulus and podocyte during development and early rapid growth periods of life are therefore likely to play significant roles in determining how and when defects in podocyte structure and function due to genetic variants become clinically manifest. Therapeutic strategies aimed at minimizing mismatch between these factors may prove clinically useful.

Indexed as

Cell CountDisease ProgressionFemaleGestational AgeGlomerulosclerosis, Focal SegmentalHumansInfantInfant, NewbornInfant, PrematureKidneyKidney Failure, ChronicKidney GlomerulusMaleOrganogenesisPodocytesGlomerular maturationGlomerular volumeGlomerulosclerosisPodocytePodocyte density

Identifiers

PMID28028615
PMCPMC5368211
OpenAlexW2563131801

What OpenQuestion holds

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LicenceCC BY
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.