Evidence map›Paper›PMID 26912542›Full record

ReviewClinical journal of the American Society of Nephrology : CJASN2016

Phosphate Toxicity in CKD: The Killer among Us.

Cynthia S Ritter, Eduardo Slatopolsky

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical journal of the American Society of Nephrology : CJASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
11.5field-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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Review
  6. Phosphate-latest news and ongoing trials.Clinical kidney journal · 2026
    Review
  7. Review
  8. Review
  9. Vitamin D and Fracture Healing.Advances in experimental medicine and biology · 2026
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Soft tissue calcifications in chronic kidney disease-beyond the vasculature.Pflugers Archiv : European journal of physiology · 2025
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Chronic Kidney Disease-associated Lung Injury Is Mediated by Phosphate-induced MAPK/AKT Signaling.American journal of respiratory cell and molecular biology · 2024
    Article

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

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

2 authors at 1 institution in 1 country.

Cynthia S RitterRenal Division, Washington University School of Medicine, St. Louis, Missouri.
Eduardo Slatopolsky
Washington University in St. Louis · US

Funding

Washington University Center for Kidney Disease ResearchP30DK079333 · NIDDK · WASHINGTON UNIVERSITY · PI HAMMERMAN, MARC RANDALL · 2007 to 2011
$5.1M
NIDDK NIH HHS P30 DK079333
6 · The paper itself

Abstract

Maintenance of a normal serum phosphate level depends on absorption in the gut, reabsorption and excretion by the kidney, and the flux between the extracellular and skeletal pools. Phosphate homeostasis is a coordinated, complex system of crosstalk between the bone, intestine, kidney, and parathyroid gland. Dysfunction of this system has serious clinical consequences in healthy individuals and those with conditions, such as CKD, in which hyperphosphatemia is associated with increased risks of cardiovascular morbidity and mortality. The last half-century of renal research has helped define the contribution of the parathyroid hormone, calcitriol, fibroblast growth factor 23, and Klotho in the regulation of phosphate. However, despite new discoveries and insights gained during this time, what remains unchanged is the recognition that phosphate retention is the initiating factor for the development of many of the complications observed in CKD, namely secondary hyperparathyroidism and bone and cardiovascular diseases. Controlling phosphate load remains the primary goal in the treatment of CKD. This review discusses the clinical effects of dysregulated phosphate metabolism, particularly in CKD, and its association with cardiovascular disease. The importance of early control of phosphate load in the treatment of CKD is emphasized, and the latest research in the treatment of phosphate retention is discussed.

Indexed as

Bone Diseases, MetabolicCardiovascular DiseasesFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseHomeostasisHumansHyperparathyroidism, SecondaryHyperphosphatemiaKlotho ProteinsPhosphatesRenal Insufficiency, ChronicFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseKlotho ProteinsPhosphatescalcitriolcardiovascular diseaseschronic kidney diseasefibroblast growth factor 23humanshyperparathyroidismhyperphosphatemiaklothoparathyroid hormonephosphatesecondary

Identifiers

PMID26912542
PMCPMC4891758
OpenAlexW2302526174

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.