Evidence map›Paper›PMID 27083280›Full record

ArticleKidney international2016

Osteopontin protects against high phosphate-induced nephrocalcinosis and vascular calcification.

Neil J Paloian, Elizabeth M Leaf, Cecilia M Giachelli

Open access · greenAbstract read
In one paragraph

Article in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 92 citations in OpenAlex.

  1. The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026
    Review
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  5. Soft tissue calcifications in chronic kidney disease-beyond the vasculature.Pflugers Archiv : European journal of physiology · 2025
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  19. Phosphate Is a Cardiovascular Toxin.Advances in experimental medicine and biology · 2022
    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 2 institutions in 1 country.

Neil J PaloianDepartment of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Elizabeth M LeafDepartment of Bioengineering, University of Washington, Seattle, Washington, USA.
Cecilia M GiachelliDepartment of Bioengineering, University of Washington, Seattle, Washington, USA. Electronic address: ceci@uw.edu.
University of Washington · USUniversity of Wisconsin–Madison · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
Pediatric Nephrology Training ProgramT32DK007662 · NIDDK · UNIVERSITY OF WASHINGTON · PI HINGORANI, SANGEETA · 1991 to 2020
$5.5M
Vascular Calcification MechanismR01HL062329 · NHLBI · UNIVERSITY OF WASHINGTON · PI GIACHELLI, CECILIA M · 1999 to 2017
$5.3M
Calcification and Vascular Cell DifferentiationR01HL081785 · NHLBI · UNIVERSITY OF WASHINGTON · PI GIACHELLI, CECILIA M · 2005 to 2017
$3.7M
Role of Osteoclastogenesis in Calcific Aortic Valve DiseaseR01HL114611 · NHLBI · UNIVERSITY OF WASHINGTON · PI GIACHELLI, CECILIA M · 2012 to 2016
$1.9M
NHLBI NIH HHS HL081785NHLBI NIH HHS HL114611NHLBI NIH HHS HL62329NHLBI NIH HHS R01 HL062329NHLBI NIH HHS R01 HL081785NHLBI NIH HHS R01 HL114611NIDDK NIH HHS 5T32DK7662-22NIDDK NIH HHS P30 DK017047NIDDK NIH HHS T32 DK007662
6 · The paper itself

Abstract

Pathologic calcification is a significant cause of increased morbidity and mortality in patients with chronic kidney disease. The precise mechanisms of ectopic calcification are not fully elucidated, but it is known to be caused by an imbalance of procalcific and anticalcific factors. In the chronic kidney disease population, an elevated phosphate burden is both highly prevalent and a known risk factor for ectopic calcification. Here we tested whether osteopontin, an inhibitor of calcification, protects against high phosphate load-induced nephrocalcinosis and vascular calcification. Osteopontin knockout mice were placed on a high phosphate diet for 11 weeks. Osteopontin deficiency together with phosphate overload caused uremia, nephrocalcinosis characterized by substantial renal tubular and interstitial calcium deposition, and marked vascular calcification when compared with control mice. Although the osteopontin-deficient mice did not exhibit hypercalcemia or hyperphosphatemia, they did show abnormalities in the mineral metabolism hormone fibroblast growth factor-23. Thus, endogenous osteopontin plays a critical role in the prevention of phosphate-induced nephrocalcinosis and vascular calcification in response to high phosphate load. A better understanding of osteopontin's role in phosphate-induced calcification will hopefully lead to better biomarkers and therapies for this disease, especially in patients with chronic kidney disease and other at-risk populations.

Indexed as

PhosphatesAnimalsAorta, AbdominalAorta, ThoracicAortic DiseasesBiomarkersBone RemodelingDietDisease Models, AnimalFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsKidneyMice, Inbred DBAMice, KnockoutNephrocalcinosisBiomarkersFibroblast Growth Factor-23Fibroblast Growth FactorsOsteopontinPhosphatesSpp1 protein, mousecalciumfibroblast growth factor-23parathyroid hormonephosphateuremiavascular calcification

Identifiers

PMID27083280
PMCPMC4834144
OpenAlexW2294532682

What OpenQuestion holds

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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.