Evidence map›Paper›PMID 36245654›Full record

ArticleKidney3602022

Critical Role of Osteopontin in Maintaining Urinary Phosphate Solubility in CKD.

Jason R Stubbs, Shiqin Zhang, Kyle P Jansson, Timothy A Fields, Joseph Boulanger, Shiguang Liu, Peter S Rowe

Open access · diamondAbstract read
In one paragraph

Article in Kidney360, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Soft tissue calcifications in chronic kidney disease-beyond the vasculature.Pflugers Archiv : European journal of physiology · 2025
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Dentoalveolar Alterations in an Adenine-Induced Chronic Kidney Disease Mouse Model.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023
    Article
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Jason R StubbsThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.ORCID 0000-0003-4580-5745
Shiqin ZhangThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.
Kyle P JanssonThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.ORCID 0000-0002-8209-2943
Timothy A FieldsThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.
Joseph BoulangerSanofi Genzyme, Cambridge, Massachusetts.
Shiguang LiuSanofi Genzyme, Cambridge, Massachusetts.
Peter S RoweThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.
University of Kansas Medical Center · USSanofi (United States) · US

Funding

Pilot and Feasibility CoreP30DK106912 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI CALVET, JAMES P · 2015 to 2019
$5.5M
Impact of Phosphaturia on Renal Osteopontin Production and PKD ProgressionR01DK122212 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Jason Stubbs, Kurt A Zimmerman · 2019 to 2026
$3.1M
The Molecular Pathology and Etiology of Nephrogenic Systemic FibrosisR01DK111693 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI ROWE, PETER S · 2017 to 2019
$689k
NIDDK NIH HHS P30 DK106912NIDDK NIH HHS R01 DK111693NIDDK NIH HHS R01 DK122212
6 · The paper itself

Abstract

Background: Nephron loss dramatically increases tubular phosphate to concentrations that exceed supersaturation. Osteopontin (OPN) is a matricellular protein that enhances mineral solubility in solution; however, the role of OPN in maintaining urinary phosphate solubility in CKD remains undefined. Methods: Here, we examined ( Results: Tubular OPN expression was dramatically increased in all studied CKD murine models. Kidney OPN gene expression and urinary OPN/Cr ratios increased before changes in traditional biochemical markers of kidney function. Moreover, a reduction of nephron numbers alone (by unilateral nephrectomy) was sufficient to induce OPN expression in residual nephrons and induction of CKD in OPN-null mice fed excess phosphate resulted in severe nephrocalcinosis. Neutralization of the ASARM motif of OPN in phosphaturic mice resulted in severe nephrocalcinosis that mimicked OPN-null CKD mice. Lastly, Conclusions: Kidney OPN expression increases in early CKD and serves a critical role in maintaining tubular mineral solubility when tubular phosphate concentrations are exceedingly high, as in late-stage CKD. Calcium-phosphate nanocrystals may be a proximal stimulus for tubular OPN production.

Indexed as

NephrocalcinosisRenal Insufficiency, ChronicAnimalsBiomarkersCalciumCalcium PhosphatesMiceMice, KnockoutOsteopontinSolubilityBiomarkersCalciumcalcium phosphateCalcium PhosphatesOsteopontinSpp1 protein, mousebasic sciencechronic kidney diseasemineral metabolismnephrocalcinosisosteopontinphosphatesolubility

Identifiers

PMID36245654
PMCPMC9528389
OpenAlexW4283372639

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.