PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

The Strategy to Prevent and Regress the Vascular Calcification in Dialysis Patients.

Abstract The high prevalence of arterial calcification in end-stage renal disease (ESRD) is far beyond the explanation by common cardiovascular risk factors such as aging, diabetes, hypertension, and dyslipidemia. The finding relies on the fact that vascular and valvular calcifications are predictors of cardiovascular diseases and mortality in persons with chronic renal failure. In addition to traditional cardiovascular risk factors such as diabetes mellitus and blood pressure control, other ESRD-related risks such as phosphate retention, excess calcium, and prolonged dialysis time also contribute to the development of vascular calcification. The strategies are to reverse "calcium paradox" and lower vascular calcification by decreasing procalcific factors including minimization of inflammation (through adequate dialysis and by avoiding malnutrition, intravenous labile iron, and positive calcium and phosphate balance), correction of high and low bone turnover, and restoration of anticalcification factor balance such as correction of vitamin D and K deficiency; parathyroid intervention is reserved for severe hyperparathyroidism. The role of bone antiresorption therapy such as bisphosphonates and denosumab in vascular calcification in high-bone-turnover disease remains unclear. The limited data on sodium thiosulfate are promising. However, if calcification is to be targeted, ensure that bone health is not compromised by the treatments.
PMID
Related Publications

Are there ways to attenuate arterial calcification and improve cardiovascular outcomes in chronic kidney disease?

Are we overconcerned about secondary hyperparathyroidism and underestimating the more common secondary hypoparathyroidism in our dialysis patients?

Biomarkers of vascular calcification and mortality in patients with ESRD.

1alpha(OH)D3 One-alpha-hydroxy-cholecalciferol--an active vitamin D analog. Clinical studies on prophylaxis and treatment of secondary hyperparathyroidism in uremic patients on chronic dialysis.

Lowering vascular calcification burden in chronic kidney disease: Is it possible?

Authors

Mayor MeshTerms

Kidney Failure, Chronic

Vascular Calcification

Keywords
Journal Title biomed research international
Publication Year Start




PMID- 28286773
OWN - NLM
STAT- MEDLINE
DA  - 20170313
DCOM- 20170317
LR  - 20170317
IS  - 2314-6141 (Electronic)
VI  - 2017
DP  - 2017
TI  - The Strategy to Prevent and Regress the Vascular Calcification in Dialysis
      Patients.
PG  - 9035193
LID - 10.1155/2017/9035193 [doi]
AB  - The high prevalence of arterial calcification in end-stage renal disease (ESRD)
      is far beyond the explanation by common cardiovascular risk factors such as
      aging, diabetes, hypertension, and dyslipidemia. The finding relies on the fact
      that vascular and valvular calcifications are predictors of cardiovascular
      diseases and mortality in persons with chronic renal failure. In addition to
      traditional cardiovascular risk factors such as diabetes mellitus and blood
      pressure control, other ESRD-related risks such as phosphate retention, excess
      calcium, and prolonged dialysis time also contribute to the development of
      vascular calcification. The strategies are to reverse "calcium paradox" and lower
      vascular calcification by decreasing procalcific factors including minimization
      of inflammation (through adequate dialysis and by avoiding malnutrition,
      intravenous labile iron, and positive calcium and phosphate balance), correction 
      of high and low bone turnover, and restoration of anticalcification factor
      balance such as correction of vitamin D and K deficiency; parathyroid
      intervention is reserved for severe hyperparathyroidism. The role of bone
      antiresorption therapy such as bisphosphonates and denosumab in vascular
      calcification in high-bone-turnover disease remains unclear. The limited data on 
      sodium thiosulfate are promising. However, if calcification is to be targeted,
      ensure that bone health is not compromised by the treatments.
FAU - Chen, Nai-Ching
AU  - Chen NC
AD  - Department of Neurology, Kaohsiung Chang Gung Memorial Hospital, Chang Gung
      University College of Medicine, Kaohsiung, Taiwan; School of Medicine, Chung Shan
      Medical University, Taichung City, Taiwan.
FAU - Hsu, Chih-Yang
AU  - Hsu CY
AUID- ORCID: 0000-0003-1151-9628
AD  - Division of Nephrology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan;
      Department of Medicine, National Yang-Ming University School of Medicine, Taipei,
      Taiwan.
FAU - Chen, Chien-Liang
AU  - Chen CL
AUID- ORCID: 0000-0002-9508-8396
AD  - Division of Nephrology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan;
      Department of Medicine, National Yang-Ming University School of Medicine, Taipei,
      Taiwan.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170214
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
RN  - 0 (Phosphates)
SB  - IM
MH  - Humans
MH  - *Kidney Failure, Chronic/blood/therapy
MH  - Phosphates/blood
MH  - Renal Dialysis/*adverse effects
MH  - Risk Factors
MH  - *Vascular Calcification/blood/etiology/prevention & control
MH  - Vitamin D Deficiency/blood/etiology/prevention & control
MH  - Vitamin K Deficiency/blood/etiology/prevention & control
PMC - PMC5329685
COI - The authors declare that there is no conflict of interests regarding the
      publication of this paper.
EDAT- 2017/03/14 06:00
MHDA- 2017/03/18 06:00
CRDT- 2017/03/14 06:00
PHST- 2016/11/17 [received]
PHST- 2017/01/17 [accepted]
AID - 10.1155/2017/9035193 [doi]
PST - ppublish
SO  - Biomed Res Int. 2017;2017:9035193. doi: 10.1155/2017/9035193. Epub 2017 Feb 14.

<?xml version="1.0" encoding="UTF-8"?>
<b:Sources SelectedStyle="" xmlns:b="http://schemas.openxmlformats.org/officeDocument/2006/bibliography"  xmlns="http://schemas.openxmlformats.org/officeDocument/2006/bibliography" >
</b:Sources>