Evidence map›Paper›PMID 25692955›Full record

ArticleKidney international2015

Differential expression and regulation of Klotho by paricalcitol in the kidney, parathyroid, and aorta of uremic rats.

Cynthia S Ritter, Sarah Zhang, James Delmez, Jane L Finch, Eduardo Slatopolsky

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Emerging concepts on the FGF23 regulation and activity.Molecular and cellular biochemistry · 2025
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  8. Review
  9. Review
  10. Review
  11. Myostatin in the Arterial Wall of Patients with End-Stage Renal Disease.Journal of atherosclerosis and thrombosis · 2020
    Article
  12. A Land of Controversy: Fibroblast Growth Factor-23 and Uremic Cardiac Hypertrophy.Journal of the American Society of Nephrology : JASN · 2020
    Review
  13. Review
  14. Klotho Gene in Human Salt-Sensitive Hypertension.Clinical journal of the American Society of Nephrology : CJASN · 2020
    Article
  15. Klotho, Aging, and the Failing Kidney.Frontiers in endocrinology · 2020
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Cynthia S RitterRenal Division, Washington University School of Medicine, St Louis, Missouri, USA.
Sarah ZhangRenal Division, Washington University School of Medicine, St Louis, Missouri, USA.
James DelmezRenal Division, Washington University School of Medicine, St Louis, Missouri, USA.
Jane L FinchRenal Division, Washington University School of Medicine, St Louis, Missouri, USA.
Eduardo SlatopolskyRenal Division, Washington University School of Medicine, St Louis, Missouri, USA.
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 DK079333NIDDK NIH HHS P30DK079333
6 · The paper itself

Abstract

Klotho plays an important role in the pathogenesis of cardiovascular disease in chronic kidney disease (CKD). Klotho is highly expressed in the kidney and parathyroid glands, but its presence in the vasculature is debated. Renal Klotho is decreased in CKD, but the effect of uremia on Klotho in other tissues is not defined. The effect of vitamin D receptor activator therapy in CKD on the expression of Klotho in various tissues is also in debate. In uremic rats (surgical 5/6th nephrectomy model), we compared 3 months of treatment with and without paricalcitol on Klotho immunostaining in the kidney, parathyroid glands, and aorta. With uremia, Klotho was unchanged in the parathyroid, significantly decreased in the kidney (66%) and the intimal-medial area of the aorta (69%), and significantly increased in the adventitial area of the aorta (67%) compared with controls. Paricalcitol prevented the decrease of Klotho in the kidney, increased expression in the parathyroid (31%), had no effect in the aortic media, but blunted the increase of Klotho in the aortic adventitia. We propose that fibroblasts are responsible for the expression of Klotho in the adventitia. In hyperplastic human parathyroid tissue from uremic patients, Klotho was higher in oxyphil compared with chief cells. Thus, under our conditions of moderate CKD and mild-to-moderate hyperphosphatemia in rats, the differential expression of Klotho and its regulation by paricalcitol in uremia is tissue-dependent.

Indexed as

AdventitiaAnimalsAortaBone Density Conservation AgentsDisease Models, AnimalErgocalciferolsFemaleFibroblastsGlucuronidaseHumansHyperparathyroidism, SecondaryHyperphosphatemiaKidneyKlotho ProteinsNephrectomyOxyphil CellsBone Density Conservation AgentsErgocalciferolsGlucuronidaseKlotho Proteinsparicalcitol

Identifiers

PMID25692955
PMCPMC4449811
OpenAlexW2026875457

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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.