Evidence map›Paper›PMID 33009821›Full record

ArticleThe Journal of pathology2021

Bedside to bench Alport syndrome research: are human urine-derived podocytes the answer?

Jin-Ju Kim, Alessia Fornoni

Open access · greenAbstract readComment
In one paragraph

Article in The Journal of pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 91% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jin-Ju KimKatz Family Division of Nephrology and Hypertension/Peggy and Harold Katz Drug Discovery Center, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA.ORCID 0000-0001-8432-7956
Alessia FornoniKatz Family Division of Nephrology and Hypertension/Peggy and Harold Katz Drug Discovery Center, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA.ORCID 0000-0002-1313-7773
University of Miami · 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
Miami Clinical and Translational Science InstituteUL1TR000460 · NCATS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SACCO, RALPH L. · 2012 to 2016
$16.9M
Crosstalk Between Lipid Droplets and Other Organelles in PodocytesR01DK104753 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FORNONI, ALESSIA · 2015 to 2025
$5.9M
Primary Outcomes in Glomerulonephritis Study (PROGRESS)UM1DK100846 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI HOLZMAN, LAWRENCE B. · 2013 to 2018
$5.8M
1/13 ApoL1 Genotypes in Kidney Donors and Long-Term Outcomes in Kidney Transplant Recipients Clinical CenterU01DK116101 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ALESSIA FORNONI, Mariella Cecilia Ortigosa-goggins · 2017 to 2026
$2.4M
(PQ12) Targeting SMPDL3b to Prevent Radiation-Induced NephrotoxicityR01CA227493 · NCI · UNIVERSITY OF ROCHESTER · PI MARPLES, BRIAN · 2018 to 2022
$2.0M
SMPDL3b and podocyte insulin signaling in DKDR01DK117599 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FORNONI, ALESSIA · 2018 to 2021
$1.4M
The role of DDR1 in podocyte lipotoxicity and progression of Alport SyndromeF32DK115109 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI KIM, JINJU · 2017 to 2019
$192k
Center for Strategic Scientific Initiatives, National Cancer Institute R01CA227493Miami clinical Translational Science Institute UL1TR000460NCATS NIH HHS UL1 TR000460NCI NIH HHS R01 CA227493NIDDK NIH HHS F32 DK115109NIDDK NIH HHS F32DK115109NIDDK NIH HHS R01 DK104753NIDDK NIH HHS R01DK104753NIDDK NIH HHS R01 DK117599NIDDK NIH HHS R01DK117599NIDDK NIH HHS U01 DK116101NIDDK NIH HHS U01DK116101NIDDK NIH HHS U54KD083912NIDDK NIH HHS UM1 DK100846NIDDK NIH HHS UM1DK100846
6 · The paper itself

Abstract

In a recent issue of The Journal of Pathology, Iampietro et al isolated and characterized several clones of urine-derived podocytes from three patients with Alport syndrome (AS) and proteinuria and one age-matched non-proteinuric control. They reported differential expression of genes involved in cell motility, adhesion, survival, and angiogenesis. The authors found AS podocytes to be less motile and to have significantly higher permeability to albumin compared to control podocytes, highlighting that AS podocytes may retain their phenotype even when losing contact with the glomerular basement membrane. The establishment of urine-derived podocyte cell lines from patients with different genetic forms of AS may represent a valuable and minimally invasive tool to investigate the cellular mechanisms contributing to kidney disease progression in AS and may allow for the establishment of patient-specific drug screening opportunities. © 2020 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Indexed as

Nephritis, HereditaryPodocytesGlomerular Basement MembraneHumansProteinuriaUnited KingdomAlport syndromecollagen IV mutationglomerular basement membraneglomerular filtration barrierurinary podocytes

Identifiers

PMID33009821
PMCPMC8142897
OpenAlexW3089704145

What OpenQuestion holds

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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.