Evidence map›Paper›PMID 22728934›Full record

ArticleThe Journal of clinical investigation2012

FGF23 neutralization improves chronic kidney disease-associated hyperparathyroidism yet increases mortality.

Victoria Shalhoub, Edward M Shatzen, Sabrina C Ward, James Davis, Jennitte Stevens, Vivian Bi, Lisa Renshaw, Nessa Hawkins, Wei Wang, Ching Chen and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 210 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
210citing papers in PubMed, 1 pooled it
21.8field-weighted citation impact, top 1% 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

210 citing papers in PubMed, 1 synthesis or guideline pooled it, 402 citations in OpenAlex.

  1. Pooled it
  2. The effects of tenapanor on serum fibroblast growth factor 23 in patients receiving hemodialysis with hyperphosphatemia.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2019
    Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Review
  9. Targeting FGF23 to Ameliorate Anemia in Chronic Kidney Disease.International journal of molecular sciences · 2026
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Unraveling the Link between Glycerol-3-Phosphate and Fibroblast Growth Factor-23 in ESKD.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Article
  15. Review
  16. Review
  17. Review
  18. Current Controversies on Adequate Circulating Vitamin D Levels in CKD.International journal of molecular sciences · 2025
    Review
  19. Multimorbidity and animal models.Animal models and experimental medicine · 2025
    Review
  20. Review

150 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 2 institutions in 1 country.

Victoria ShalhoubDepartment of Metabolic Disorders, Amgen Inc., Thousand Oaks, CA, USA.
Edward M Shatzen
Sabrina C Ward
James Davis
Jennitte Stevens
Vivian Bi
Lisa Renshaw
Nessa Hawkins
Wei Wang
Ching Chen
Mei-Mei Tsai
Russell C Cattley
Thomas J Wronski
Xuechen Xia
Xiaodong Li
Charles Henley
Michael Eschenberg
William G Richards
Amgen (United States) · USUniversity of Florida · US

Funding

UF Clinical and Translational Science AwardUL1TR000064 · NCATS · UNIVERSITY OF FLORIDA · PI NELSON, DAVID R · 2012 to 2014
$12.2M
NCATS NIH HHS UL1 TR000064
6 · The paper itself

Abstract

Chronic kidney disease-mineral and bone disorder (CKD-MBD) is associated with secondary hyperparathyroidism (HPT) and serum elevations in the phosphaturic hormone FGF23, which may be maladaptive and lead to increased morbidity and mortality. To determine the role of FGF23 in the pathogenesis of CKD-MBD and development of secondary HPT, we developed a monoclonal FGF23 antibody to evaluate the impact of chronic FGF23 neutralization on CKD-MBD, secondary HPT, and associated comorbidities in a rat model of CKD-MBD. CKD-MBD rats fed a high-phosphate diet were treated with low or high doses of FGF23-Ab or an isotype control antibody. Neutralization of FGF23 led to sustained reductions in secondary HPT, including decreased parathyroid hormone, increased vitamin D, increased serum calcium, and normalization of bone markers such as cancellous bone volume, trabecular number, osteoblast surface, osteoid surface, and bone-formation rate. In addition, we observed dose-dependent increases in serum phosphate and aortic calcification associated with increased risk of mortality in CKD-MBD rats treated with FGF23-Ab. Thus, mineral disturbances caused by neutralization of FGF23 limited the efficacy of FGF23-Ab and likely contributed to the increased mortality observed in this CKD-MBD rat model.

Indexed as

AnimalsAntibodies, Monoclonal, Murine-DerivedAortaBiomarkersCalcitriolCalciumCHO CellsChronic Kidney Disease-Mineral and Bone DisorderCricetinaeFibroblast Growth Factor-23Fibroblast Growth FactorsGenes, ReporterGlomerular Filtration RateHemodynamicsHyperparathyroidism, SecondaryKidneyAntibodies, Monoclonal, Murine-DerivedBiomarkersCalcitriolCalciumFgf23 protein, mouseFgf23 protein, ratFibroblast Growth Factor-23Fibroblast Growth FactorsLuciferasesParathyroid HormonePhosphates

Identifiers

PMID22728934
PMCPMC3386816
OpenAlexW2078730571

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.