Evidence map›Paper›PMID 27992580›Full record

ArticlePloS one2016

Urinary Podocyte Loss Is Increased in Patients with Fabry Disease and Correlates with Clinical Severity of Fabry Nephropathy.

Brent Fall, C Ronald Scott, Michael Mauer, Stuart Shankland, Jeffrey Pippin, Jonathan A Jefferson, Eric Wallace, David Warnock, Behzad Najafian

2 registry-linked trialsAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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.

NCT02994303 unknown statusnot on this map

Podocyturia, a Non-Invasive Predictor of Renal Dysfunction in Fabry Nephropathy

TypeobservationalSponsorUniversity of WashingtonRan2014 to 2019Enrolled58ConditionsFabry Disease
NCT06325488 recruitingnot on this mapstarted 2024, after this paper: background citation

Fibrosis, Inflammation, Oxygenation of Renal Tissue In FabrY Disease

TypeobservationalSponsorCaroline Michaela KistorpRan2024 to 2026Enrolled60ConditionsFabry Disease, Chronic Kidney Diseases
3 · Its place in the literature

Who cites it

33 citing papers in PubMed.

  1. Trial
  2. NovelJournal of clinical medicine · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Arrhythmogenesis in Fabry Disease.Current cardiology reports · 2024
    Review
  9. Article
  10. Glomerular hyperfiltration.Nature reviews. Nephrology · 2022
    Review
  11. Implications of Sphingolipid Metabolites in Kidney Diseases.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Renal Manifestations of Fabry Disease: A Narrative Review.Canadian journal of kidney health and disease · 2021
    Review
  18. Review
  19. 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

9 authors.

Brent FallDepartment of Pathology, University of Washington, Seattle, United States America.
C Ronald ScottDepartment of Pediatrics, University of Washington, Seattle, United States America.
Michael MauerDepartments of Pediatrics, University of Minnesota, Minneapolis, United States America.
Stuart ShanklandDepartment of Medicine, University of Washington, Seattle, United States America.
Jeffrey PippinDepartment of Medicine, University of Washington, Seattle, United States America.
Jonathan A JeffersonDepartment of Medicine, University of Washington, Seattle, United States America.
Eric WallaceDepartment of Medicine, University of Alabama, Birmingham, United States America.
David WarnockDepartment of Medicine, University of Alabama, Birmingham, United States America.
Behzad NajafianDepartment of Pathology, University of Washington, Seattle, United States America.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease is a major complication of Fabry disease. Podocytes accumulate globotriaosylceramide inclusions more than other kidney cell types in Fabry patients. Podocyte injury occurs early in age, and is progressive. Since injured podocytes detach into the urine (podocyturia), we hypothesized that podocyturia would increase in Fabry patients and correlate with clinical severity of Fabry nephropathy. Urine specimens from 39 Fabry patients and 24 healthy subjects were evaluated for podocyturia. Most of the Fabry patients and many healthy subjects had podocyturia. The number of podocytes per gram of urine creatinine (UPodo/g Cr) was 3.6 fold greater in Fabry patients (3,741 ± 2796; p = 0.001) than healthy subjects (1,040 ± 972). Fabry patients with normoalbuminuria and normoproteinuria had over 2-fold greater UPodo/g Cr than healthy subjects (p = 0.048). UPodo/gCr was inversely related to eGFR in male patients (r = -0.69, p = 0.003). UPodo/gCr was directly related to urine protein creatinine ratio (r = 0.33; p = 0.04) in all Fabry patients. These studies confirm increased podocyturia in Fabry disease, even when proteinuria and albuminuria are absent. Podocyturia correlates with clinical severity of Fabry nephropathy, and potentially may be of prognostic value.

Indexed as

AdolescentAdultAgedCase-Control StudiesChildChild, PreschoolDisease ProgressionFabry DiseaseFemaleHumansMaleMiddle AgedPodocytesPrognosisProteinuriaRenal Insufficiency, Chronic

Identifiers

PMID27992580
PMCPMC5161377

What OpenQuestion holds

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Registered trials

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.