Evidence map›Paper›PMID 28704395›Full record

ArticlePloS one2017

Intraperitoneal pyrophosphate treatment reduces renal calcifications in Npt2a null mice.

Daniel Caballero, Yuwen Li, Jonathan Fetene, Julian Ponsetto, Alyssa Chen, Chuanlong Zhu, Demetrios T Braddock, Clemens Bergwitz

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Hypophosphatemic rickets: diagnosis and treatment.Archives of endocrinology and metabolism · 2026
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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

8 authors at 3 institutions in 2 countries.

Daniel CaballeroDepartment of Medicine, Section Endocrinology, Yale University School of Medicine, New Haven, CT, United States of America.
Yuwen LiEndocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, United States of America.
Jonathan FeteneDepartment of Medicine, Section Endocrinology, Yale University School of Medicine, New Haven, CT, United States of America.
Julian PonsettoDepartment of Medicine, Section Endocrinology, Yale University School of Medicine, New Haven, CT, United States of America.
Alyssa ChenDepartment of Medicine, Section Endocrinology, Yale University School of Medicine, New Haven, CT, United States of America.
Chuanlong ZhuGastroenterology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, United States of America.
Demetrios T BraddockDepartment of Pathology, Yale University School of Medicine, New Haven, CT, United States of America.
Clemens BergwitzDepartment of Medicine, Section Endocrinology, Yale University School of Medicine, New Haven, CT, United States of America.ORCID http://orcid.org/0000-0002-7518-249X
Yale University · USBoston University · USHarvard University · US

Funding

Renal Physiology and Phenotyping CoreP30DK079310 · NIDDK · YALE UNIVERSITY · PI ARONSON, PETER S. · 2008 to 2022
$16.8M
Yale Mouse Metabolic Phenotyping CenterU24DK059635 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 2001 to 2015
$8.9M
Skeletal Phenotyping CoreP30AR066261 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DIVIETI PAJEVIC, PAOLA · 2014 to 2018
$3.5M
Role of the renal sodium-phosphate co-transporter NaPi-IIc in phosphate homeostasK08DK078361 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BERGWITZ, CLEMENS · 2007 to 2011
$741k
NIAMS NIH HHS P30 AR066261NIDDK NIH HHS K08 DK078361NIDDK NIH HHS P30 DK079310NIDDK NIH HHS U24 DK059635
6 · The paper itself

Abstract

Mutations in the proximal tubular sodium-dependent phosphate co-transporters NPT2a and NPT2c have been reported in patients with renal stone disease and nephrocalcinosis, however the relative contribution of genotype, dietary calcium and phosphate, and modifiers of mineralization such as pyrophosphate (PPi) to the formation of renal mineral deposits is unclear. In the present study, we used Npt2a-/- mice to model the renal calcifications observed in these disorders. We observed elevated urinary excretion of PPi in Npt2a-/- mice when compared to WT mice. Presence of two hypomorphic Extracellular nucleotide pyrophosphatase phosphodiesterase 1 (Enpp1asj/asj) alleles decreased urine PPi and worsened renal calcifications in Npt2a-/- mice. These studies suggest that PPi is a thus far unrecognized factor protecting Npt2a-/- mice from the development of renal mineral deposits. Consistent with this conclusion, we next showed that renal calcifications in these mice can be reduced by intraperitoneal administration of sodium pyrophosphate. If confirmed in humans, urine PPi could therefore be of interest for developing new strategies to prevent the nephrocalcinosis and nephrolithiasis seen in phosphaturic disorders.

Indexed as

AnimalsDiphosphatesDisease Models, AnimalFemaleHumansInjections, IntraperitonealKidney CalculiMaleMiceMice, KnockoutMutationPhosphoric Diester HydrolasesPyrophosphatasesSodium-Phosphate Cotransporter Proteins, Type IIaTreatment OutcomeDiphosphatesdiphosphoric acidectonucleotide pyrophosphatase phosphodiesterase 1Phosphoric Diester HydrolasesPyrophosphatasesSlc34a1 protein, mouseSodium-Phosphate Cotransporter Proteins, Type IIasodium pyrophosphate

Identifiers

PMID28704395
PMCPMC5509111
OpenAlexW2736060939

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.