Evidence map›Paper›PMID 25568173›Full record

ArticleJournal of the American Society of Nephrology : JASN2015

Human Urine-Derived Renal Progenitors for Personalized Modeling of Genetic Kidney Disorders.

Elena Lazzeri, Elisa Ronconi, Maria Lucia Angelotti, Anna Peired, Benedetta Mazzinghi, Francesca Becherucci, Sara Conti, Giulia Sansavini, Alessandro Sisti, Fiammetta Ravaglia and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 103 citations in OpenAlex.

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  11. Role of mitochondria in endogenous renal repair.Clinical science (London, England : 1979) · 2024
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  17. p16Lupus science & medicine · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 5 institutions in 3 countries.

Elena LazzeriExcellence Centre for Research, Transfer and High Education for the Development of DE NOVO Therapies (DENOTHE) and paola.romagnani@unifi.it elena.lazzeri@unifi.it.
Elisa RonconiExcellence Centre for Research, Transfer and High Education for the Development of DE NOVO Therapies (DENOTHE) and Department of Clinical and Experimental Biomedical Sciences, University of Florence, Florence, Italy;
Maria Lucia AngelottiExcellence Centre for Research, Transfer and High Education for the Development of DE NOVO Therapies (DENOTHE) and.
Anna PeiredExcellence Centre for Research, Transfer and High Education for the Development of DE NOVO Therapies (DENOTHE) and Department of Clinical and Experimental Biomedical Sciences, University of Florence, Florence, Italy;
Benedetta MazzinghiMedical Genetics Unit and.
Francesca BecherucciPediatric Nephrology Unit, Meyer Children's University Hospital, Florence, Italy;
Sara ContiIRCCS-Istituto di Ricerche Farmacologiche "Mario Negri," Centro Anna Maria Astori, Bergamo, Italy; and.
Giulia SansaviniPediatric Nephrology Unit, Meyer Children's University Hospital, Florence, Italy;
Alessandro SistiExcellence Centre for Research, Transfer and High Education for the Development of DE NOVO Therapies (DENOTHE) and.
Fiammetta RavagliaPediatric Nephrology Unit, Meyer Children's University Hospital, Florence, Italy;
Duccio LombardiExcellence Centre for Research, Transfer and High Education for the Development of DE NOVO Therapies (DENOTHE) and.
Aldesia ProvenzanoMedical Genetics Unit and.
Anna ManonellesDepartment of Nephrology, Bellvitge's University Hospital, Barcelona, Spain.
Josep M CruzadoDepartment of Nephrology, Bellvitge's University Hospital, Barcelona, Spain.
Sabrina GiglioDepartment of Clinical and Experimental Biomedical Sciences, University of Florence, Florence, Italy; Medical Genetics Unit and.
Rosa Maria RopertoPediatric Nephrology Unit, Meyer Children's University Hospital, Florence, Italy;
Marco MaterassiPediatric Nephrology Unit, Meyer Children's University Hospital, Florence, Italy;
Laura LasagniExcellence Centre for Research, Transfer and High Education for the Development of DE NOVO Therapies (DENOTHE) and.
Paola RomagnaniExcellence Centre for Research, Transfer and High Education for the Development of DE NOVO Therapies (DENOTHE) and Department of Clinical and Experimental Biomedical Sciences, University of Florence, Florence, Italy; Pediatric Nephrology Unit, Meyer Children's University Hospital, Florence, Italy; paola.romagnani@unifi.it elena.lazzeri@unifi.it.
Meyer Children's Hospital · ITUniversity of Florence · ITMedical Genetics Center · DEBellvitge University Hospital · ESMario Negri Institute for Pharmacological Research · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The critical role of genetic and epigenetic factors in the pathogenesis of kidney disorders is gradually becoming clear, and the need for disease models that recapitulate human kidney disorders in a personalized manner is paramount. In this study, we describe a method to select and amplify renal progenitor cultures from the urine of patients with kidney disorders. Urine-derived human renal progenitors exhibited phenotype and functional properties identical to those purified from kidney tissue, including the capacity to differentiate into tubular cells and podocytes, as demonstrated by confocal microscopy, Western blot analysis of podocyte-specific proteins, and scanning electron microscopy. Lineage tracing studies performed with conditional transgenic mice, in which podocytes are irreversibly tagged upon tamoxifen treatment (NPHS2.iCreER;mT/mG), that were subjected to doxorubicin nephropathy demonstrated that renal progenitors are the only urinary cell population that can be amplified in long-term culture. To validate the use of these cells for personalized modeling of kidney disorders, renal progenitors were obtained from (1) the urine of children with nephrotic syndrome and carrying potentially pathogenic mutations in genes encoding for podocyte proteins and (2) the urine of children without genetic alterations, as validated by next-generation sequencing. Renal progenitors obtained from patients carrying pathogenic mutations generated podocytes that exhibited an abnormal cytoskeleton structure and functional abnormalities compared with those obtained from patients with proteinuria but without genetic mutations. The results of this study demonstrate that urine-derived patient-specific renal progenitor cultures may be an innovative research tool for modeling of genetic kidney disorders.

Indexed as

Cell Culture TechniquesAdolescentAnimalsCase-Control StudiesChildChild, PreschoolFemaleHumansInfantKidneyKidney DiseasesMaleMice, Inbred BALB CMice, SCIDMice, TransgenicStem Cellsglomerulonephritisglomerulosclerosiskidneymutationnext generationpodocytes

Identifiers

PMID25568173
PMCPMC4520157
OpenAlexW2160695955

What OpenQuestion holds

Textmetadata
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.