Evidence map›Paper›PMID 23967103›Full record

ArticlePloS one2013

Renal expression of FGF23 in progressive renal disease of diabetes and the effect of ACE inhibitor.

Cristina Zanchi, Monica Locatelli, Ariela Benigni, Daniela Corna, Susanna Tomasoni, Daniela Rottoli, Flavio Gaspari, Giuseppe Remuzzi, Carlamaria Zoja

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.5field-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

45 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Nephroprotective Effects ofCurrent issues in molecular biology · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Strategies to lower fibroblast growth factor 23 bioactivity.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Biology of Fibroblast Growth Factor 23: From Physiology to Pathology.Cold Spring Harbor perspectives in medicine · 2018
    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 at 2 institutions in 1 country.

Cristina ZanchiIRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy.
Monica Locatelli
Ariela Benigni
Daniela Corna
Susanna Tomasoni
Daniela Rottoli
Flavio Gaspari
Giuseppe Remuzzi
Carlamaria Zoja
Mario Negri Institute for Pharmacological Research · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone mainly produced by bone that acts in the kidney through FGF receptors and Klotho. Here we investigated whether the kidney was an additional source of FGF23 during renal disease using a model of type 2 diabetic nephropathy. Renal expression of FGF23 and Klotho was assessed in Zucker diabetic fatty (ZDF) and control lean rats at 2, 4, 6, 8 months of age. To evaluate whether the renoprotective effect of angiotensin converting enzyme (ACE) inhibitor in this model was associated with changes in FGF23 and Klotho, ZDF rats received ramipril from 4, when proteinuric, to 8 months of age. FGF23 mRNA was not detectable in the kidney of lean rats, nor of ZDF rats at 2 months of age. FGF23 became measurable in the kidney of diabetic rats at 4 months and significantly increased thereafter. FGF23 protein localized in proximal and distal tubules. Renal Klotho mRNA and protein decreased during time in ZDF rats. As renal disease progressed, serum phosphate levels increased in parallel with decline of fractional phosphorus excretion. Ramipril limited proteinuria and renal injury, attenuated renal FGF23 upregulation and ameliorated Klotho expression. Ramipril normalized serum phosphate levels and tended to increase fractional phosphorus excretion. These data indicate that during progressive renal disease the kidney is a site of FGF23 production which is limited by ACE inhibition. Interfering pharmacologically with the delicate balance of FGF23 and phosphorus in diabetes may have implications in clinics.

Indexed as

Disease ProgressionAngiotensin-Converting Enzyme InhibitorsAnimalsCytoprotectionDiabetes Mellitus, Type 2Fibroblast Growth FactorsGene Expression RegulationGlucuronidaseKidneyKlotho ProteinsMalePeptidyl-Dipeptidase APhosphatesRatsSodium-Phosphate Cotransporter ProteinsAngiotensin-Converting Enzyme InhibitorsFgf23 protein, ratFibroblast Growth FactorsGlucuronidaseKlotho ProteinsPeptidyl-Dipeptidase APhosphatesSodium-Phosphate Cotransporter Proteins

Identifiers

PMID23967103
PMCPMC3743899
OpenAlexW1986017413

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.