Evidence map›Paper›PMID 25136676›Full record

ReviewTheScientificWorldJournal2014

Vascular calcification and renal bone disorders.

Kuo-Cheng Lu, Chia-Chao Wu, Jen-Fen Yen, Wen-Chih Liu

Open access · goldAbstract readReview
In one paragraph

Review in TheScientificWorldJournal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
  2. Trial
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  4. Article
  5. Review
  6. Article
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  9. Article
  10. Article
  11. Regulatory Role of Sex Hormones in Cardiovascular Calcification.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Research Models for Studying Vascular Calcification.International journal of molecular sciences · 2020
    Review
  14. Article
  15. Review
  16. Observational
  17. Article
  18. Review
  19. Review
  20. Epithelial Cell Cycle Behaviour in the Injured Kidney.International journal of molecular sciences · 2018
    Review
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

4 authors at 3 institutions in 1 country.

Kuo-Cheng LuDivision of Nephrology, Department of Medicine, Cardinal Tien Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 23148, Taiwan.
Chia-Chao WuDivision of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan.
Jen-Fen YenDivision of Nephrology, Department of Internal Medicine, Yonghe Cardinal Tien Hospital, 80 Zhongxing Street, Yonghe District, New Taipei City 23445, Taiwan.
Wen-Chih LiuDivision of Nephrology, Department of Internal Medicine, Yonghe Cardinal Tien Hospital, 80 Zhongxing Street, Yonghe District, New Taipei City 23445, Taiwan.
Cardinal Tien Hospital · TWFu Jen Catholic University · TWNational Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At the early stage of chronic kidney disease (CKD), the systemic mineral metabolism and bone composition start to change. This alteration is known as chronic kidney disease-mineral bone disorder (CKD-MBD). It is well known that the bone turnover disorder is the most common complication of CKD-MBD. Besides, CKD patients usually suffer from vascular calcification (VC), which is highly associated with mortality. Many factors regulate the VC mechanism, which include imbalances in serum calcium and phosphate, systemic inflammation, RANK/RANKL/OPG triad, aldosterone, microRNAs, osteogenic transdifferentiation, and effects of vitamins. These factors have roles in both promoting and inhibiting VC. Patients with CKD usually have bone turnover problems. Patients with high bone turnover have increase of calcium and phosphate release from the bone. By contrast, when bone turnover is low, serum calcium and phosphate levels are frequently maintained at high levels because the reservoir functions of bone decrease. Both of these conditions will increase the possibility of VC. In addition, the calcified vessel may secrete FGF23 and Wnt inhibitors such as sclerostin, DKK-1, and secreted frizzled-related protein to prevent further VC. However, all of them may fight back the inhibition of bone formation resulting in fragile bone. There are several ways to treat VC depending on the bone turnover status of the individual. The main goals of therapy are to maintain normal bone turnover and protect against VC.

Indexed as

AnimalsChronic Kidney Disease-Mineral and Bone DisorderFibroblast Growth Factor-23HumansRenal Insufficiency, ChronicVascular CalcificationFibroblast Growth Factor-23

Identifiers

PMID25136676
PMCPMC4127293
OpenAlexW2048536527

What OpenQuestion holds

Textmetadata
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.