Evidence map›Paper›PMID 23344574›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Increased biological response to 1,25(OH)(2)D(3) in genetic hypercalciuric stone-forming rats.

Kevin K Frick, John R Asplin, Murray J Favus, Christopher Culbertson, Nancy S Krieger, David A Bushinsky

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

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  16. Effect of Potassium Citrate on Calcium Phosphate Stones in a Model of Hypercalciuria.Journal of the American Society of Nephrology : JASN · 2015
    Article
  17. Modeling hypercalciuria in the genetic hypercalciuric stone-forming rat.Current opinion in nephrology and hypertension · 2015
    Review
  18. Article
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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

6 authors at 3 institutions in 1 country.

Kevin K FrickDivision of Nephrology, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA. Kevin_Frick@URMC.Rochester.edu
John R Asplin
Murray J Favus
Christopher Culbertson
Nancy S Krieger
David A Bushinsky
University of Rochester · USLink Foundation · USUniversity of Chicago · US

Funding

Hypercalciuria and Bone Quality in the Genetic Hypercalciuric Stone-Forming RatsR01DK075462 · NIDDK · UNIVERSITY OF ROCHESTER · PI BUSHINSKY, DAVID A · 2008 to 2019
$3.8M
NIDDK NIH HHS R01 DK075462NIDDK NIH HHS R01-DK-075462
6 · The paper itself

Abstract

Genetic hypercalciuric stone-forming (GHS) rats, bred to maximize urine (U) calcium (Ca) excretion, have increased intestinal Ca absorption and bone Ca resorption and reduced renal Ca reabsorption, leading to increased UCa compared with the Sprague-Dawley (SD) rats. GHS rats have increased vitamin D receptors (VDR) at each of these sites, with normal levels of 1,25(OH)(2)D(3) (1,25D), indicating that their VDR is undersaturated with 1,25D. We tested the hypothesis that 1,25D would induce a greater increase in UCa in GHS rats by feeding both strains ample Ca and injecting 1,25D (25 ng · 100 g body wt(-1) · day(-1)) or vehicle for 16 days. With 1,25D, UCa in SD increased from 1.7 ± 0.3 mg/day to 24.4 ± 1.2 (Δ = 22.4 ± 1.5) and increased more in GHS from 10.5 ± 0.7 to 41.9 ± 0.7 (Δ = 29.8 ± 1.8; P = 0.003). To determine the mechanism of the greater increase in UCa in GHS rats, we measured kidney RNA expression of components of renal Ca transport. Expression of transient receptor potential vanilloid (TRPV)5 and calbindin D(28K) were increased similarly in SD + 1,25D and GHS + 1,25D. The Na(+)/Ca(2+) exchanger (NCX1) was increased in GHS + 1,25D. Klotho was decreased in SD + 1,25D and GHS + 1,25D. TRPV6 was increased in SD + 1,25D and increased further in GHS + 1,25D. Claudin 14, 16, and 19, Na/K/2Cl transporter (NKCC2), and secretory K channel (ROMK) did not differ between SD + 1,25D and GHS + 1,25D. Increased UCa with 1,25D in GHS exceeded that of SD, indicating that the increased VDR in GHS induces a greater biological response. This increase in UCa, which must come from the intestine and/or bone, must exceed any effect of 1,25D on TRPV6 or NCX1-mediated renal Ca reabsorption.

Indexed as

AnimalsBiomarkersCalcitriolCalciumCalcium OxalateCalcium PhosphatesDisease Models, AnimalHypercalcemiaHypercalciuriaKidneyKidney CalculiMaleRatsRats, Sprague-DawleyBiomarkersCalcitriolCalciumCalcium Oxalatecalcium phosphate, dibasic, anhydrousCalcium Phosphates

Identifiers

PMID23344574
PMCPMC3602696
OpenAlexW2064633413

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.