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Role of Vitamin D in Uremic Vascular Calcification.

Abstract The risk of cardiovascular death is 10 times higher in patients with CKD (chronic kidney disease) than in those without CKD. Vascular calcification, common in patients with CKD, is a predictor of cardiovascular mortality. Vitamin D deficiency, another complication of CKD, is associated with vascular calcification in patients with CKD. GFR decline, proteinuria, tubulointerstitial injury, and the therapeutic dose of active form vitamin D aggravate vitamin D deficiency and reduce its pleiotropic effect on the cardiovascular system. Vitamin D supplement for CKD patients provides a protective role in vascular calcification on the endothelium by (1) renin-angiotensin-aldosterone system inactivation, (2) alleviating insulin resistance, (3) reduction of cholesterol and inhibition of foam cell and cholesterol efflux in macrophages, and (4) modulating vascular regeneration. For the arterial calcification, vitamin D supplement provides adjunctive role in regressing proteinuria, reverse renal osteodystrophy, and restoring calcification inhibitors. Recently, adventitial progenitor cell has been linked to be involved in the vascular calcification. Vitamin D may provide a role in modulating adventitial progenitor cells. In summary, vitamin D supplement may provide an ancillary role for ameliorating uremic vascular calcification.
PMID
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Authors

Mayor MeshTerms

Endothelium, Vascular

Renal Insufficiency, Chronic

Uremia

Vascular Calcification

Keywords
Journal Title biomed research international
Publication Year Start




PMID- 28286758
OWN - NLM
STAT- MEDLINE
DA  - 20170313
DCOM- 20170317
LR  - 20170317
IS  - 2314-6141 (Electronic)
VI  - 2017
DP  - 2017
TI  - Role of Vitamin D in Uremic Vascular Calcification.
PG  - 2803579
LID - 10.1155/2017/2803579 [doi]
AB  - The risk of cardiovascular death is 10 times higher in patients with CKD (chronic
      kidney disease) than in those without CKD. Vascular calcification, common in
      patients with CKD, is a predictor of cardiovascular mortality. Vitamin D
      deficiency, another complication of CKD, is associated with vascular
      calcification in patients with CKD. GFR decline, proteinuria, tubulointerstitial 
      injury, and the therapeutic dose of active form vitamin D aggravate vitamin D
      deficiency and reduce its pleiotropic effect on the cardiovascular system.
      Vitamin D supplement for CKD patients provides a protective role in vascular
      calcification on the endothelium by (1) renin-angiotensin-aldosterone system
      inactivation, (2) alleviating insulin resistance, (3) reduction of cholesterol
      and inhibition of foam cell and cholesterol efflux in macrophages, and (4)
      modulating vascular regeneration. For the arterial calcification, vitamin D
      supplement provides adjunctive role in regressing proteinuria, reverse renal
      osteodystrophy, and restoring calcification inhibitors. Recently, adventitial
      progenitor cell has been linked to be involved in the vascular calcification.
      Vitamin D may provide a role in modulating adventitial progenitor cells. In
      summary, vitamin D supplement may provide an ancillary role for ameliorating
      uremic vascular calcification.
FAU - Hou, Yi-Chou
AU  - Hou YC
AUID- ORCID: 0000-0001-7662-9890
AD  - Division of Nephrology, Department of Internal Medicine, Cardinal Tien Hospital, 
      School of Medicine, Fu-Jen Catholic University, New Taipei City, Taiwan.
FAU - Liu, Wen-Chih
AU  - Liu WC
AUID- ORCID: 0000-0002-6778-9670
AD  - Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical
      University, Taipei, Taiwan; Division of Nephrology, Department of Internal
      Medicine, Yonghe Cardinal Tien Hospital, New Taipei City, Taiwan.
FAU - Zheng, Cai-Mei
AU  - Zheng CM
AUID- ORCID: 0000-0003-0370-3951
AD  - Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical
      University, Taipei, Taiwan; Department of Internal Medicine, School of Medicine, 
      College of Medicine, Taipei Medical University, Taipei, Taiwan; Division of
      Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical
      University, New Taipei City, Taiwan.
FAU - Zheng, Jing-Quan
AU  - Zheng JQ
AD  - Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical
      University, Taipei, Taiwan; Division of Critical Care Medicine, Department of
      Emergency Medicine-Critical Care Medicine (EM-CCM), Shuang Ho Hospital, Taipei
      Medical University, New Taipei City, Taiwan.
FAU - Yen, Tzung-Hai
AU  - Yen TH
AUID- ORCID: 0000-0002-0907-1505
AD  - Department of Nephrology and Division of Clinical Toxicology and Toxicology
      Laboratory, Chang Gung Memorial Hospital, Linkou Medical Center, Taoyuan, Taiwan.
FAU - Lu, Kuo-Cheng
AU  - Lu KC
AUID- ORCID: 0000-0002-7062-8560
AD  - Division of Nephrology, Department of Internal Medicine, Cardinal Tien Hospital, 
      School of Medicine, Fu-Jen Catholic University, New Taipei City, Taiwan; Graduate
      Institute of Clinical Medicine, College of Medicine, Taipei Medical University,
      Taipei, Taiwan; Division of Nephrology, Department of Medicine, Tri-Service
      General Hospital, National Defense Medical Center, Taipei, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170212
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
RN  - 1406-16-2 (Vitamin D)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Adventitia/metabolism/pathology
MH  - Animals
MH  - Cholesterol/metabolism
MH  - *Endothelium, Vascular/metabolism/pathology
MH  - Foam Cells/metabolism/pathology
MH  - Humans
MH  - Insulin Resistance
MH  - *Renal Insufficiency, Chronic/complications/drug therapy/metabolism/pathology
MH  - Renin-Angiotensin System/drug effects
MH  - *Uremia/complications/drug therapy/metabolism/pathology
MH  - *Vascular Calcification/drug therapy/etiology/metabolism/pathology
MH  - Vitamin D/*therapeutic use
PMC - PMC5329659
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- 2016/11/01 [received]
PHST- 2016/12/26 [revised]
PHST- 2017/01/16 [accepted]
AID - 10.1155/2017/2803579 [doi]
PST - ppublish
SO  - Biomed Res Int. 2017;2017:2803579. doi: 10.1155/2017/2803579. Epub 2017 Feb 12.

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