Evidence map›Paper›PMID 19195964›Full record

ArticleArchives of pathology & laboratory medicine2009

Advances in the biology and genetics of the podocytopathies: implications for diagnosis and therapy.

Laura Barisoni, H William Schnaper, Jeffrey B Kopp

Open access · greenAbstract read
In one paragraph

Article in Archives of pathology & laboratory medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 99 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Review
  7. Genetic Susceptibility to Chronic Kidney Disease: Links, Risks and Management.International journal of nephrology and renovascular disease · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Similar Biophysical Abnormalities in Glomeruli and Podocytes from Two Distinct Models.Journal of the American Society of Nephrology : JASN · 2018
    Article
  16. Prospects for Precision Medicine in Glomerulonephritis Treatment.Canadian journal of kidney health and disease · 2018
    Review
  17. Review
  18. Reproducibility of the NEPTUNE descriptor-based scoring system on whole-slide images and histologic and ultrastructural digital images.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016
    Article
  19. Podocytes.F1000Research · 2016
    Review
  20. Article
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

3 authors at 1 institution in 1 country.

Laura BarisoniDepartment of Pathology and Medicine, Division of Nephrology, New York University School of Medicine, New York, NY 10017, USA. barisol01@med.nyu.edu
H William Schnaper
Jeffrey B Kopp
National Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

MULTIDISCIPLINARY CLINICAL AND TRANSLATIONAL SCIENCE (MCTS) PROGRAM (UL1)UL1RR025741 · NCRR · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GREENLAND, PHILIP · 2008 to 2011
$24.7M
Focal Segmental Glomerulosclerosis: Genetics & MechanismsZIADK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2009 to 2024
$15.7M
Focal segmental glomerulosclerosis: TreatmentZIADK043412 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2009 to 2024
$7.4M
Focal segmental glomerulosclerosis: HIV-associated nephropathyZIADK043411 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HEYMANN, JURGEN · 2009 to 2024
$7.3M
FOCAL SEGMENTAL GLOMERULOSCLEROSIS--PATHOGENESIS AND TREATMENTZ01DK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 1997 to 2008
$1.0M
Intramural NIH HHS Z01 DK043308NCRR NIH HHS UL1 RR025741
6 · The paper itself

Abstract

contextEtiologic factors and pathways leading to altered podocyte phenotype are clearly numerous and involve the activity of different cellular function.

objectiveTo focus on recent discoveries in podocyte biology and genetics and their relevance to these human glomerular diseases, named podocytopathies. DATA SOURCES: Genetic mutations in genes encoding for proteins in the nucleus, slit diaphragm, podocyte cytoplasm, and cell membrane are responsible for podocyte phenotype and functional abnormalities. Podocyte injury may also derive from secondary stimuli, such as mechanical stress, infections, or use of certain medications. Podocytes can respond to injury in a limited number of ways, which include (1) effacement, (2) apoptosis, (3) arrest of development, and (4) dedifferentiation. Each of these pathways results in a specific glomerular morphology: minimal change nephropathy, focal segmental glomerulosclerosis, diffuse mesangial sclerosis, and collapsing glomerulopathy.

conclusionsBased on current knowledge of podocyte biology, we organized etiologic factors and morphologic features in a taxonomy of podocytopathies, which provides a novel approach to the classification of these diseases. Current and experimental therapeutic approaches are also discussed.

Indexed as

ApoptosisCell DifferentiationCell ProliferationHumansKidney DiseasesMutationPodocytes

Identifiers

PMID19195964
PMCPMC3118840
OpenAlexW1511867626

What OpenQuestion holds

Textmetadata
LicenceTDM
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.