Inflammation and vascular calcification

Research output: Contribution to journalArticle

82 Citations (Scopus)

Abstract

Both vascular calcification and inflammation are common in patients with chronic kidney disease (CKD). In patients on dialysis, there is increased coronary artery and peripheral artery calcification compared to the general population. Both intimal (atherosclerotic) and medial calcification in CKD patients are associated with increased morbidity and mortality. Vascular calcification is an active cell-mediated process, and likely reflects a transformation of vascular smooth muscle cells to osteoblast-like cells. Pooled uremic serum can induce this transformation, but the mechanism by which it does so is not yet clear. Several mediators of inflammation such as oxidation, carbonyl stress, C-reactive protein, and cytokines may directly stimulate vascular calcification. In addition, inflammation itself reduces fetuin-A, a naturally occurring inhibitor of vascular calcification which binds excess mineral in serum. The combination of the acceleration of vascular calcification together with impaired defense mechanisms creates a uremic milieu primed for extra-osseous calcification.

Original languageEnglish
Pages (from-to)64-71
Number of pages8
JournalBlood Purification
Volume23
Issue number1
DOIs
StatePublished - 2005

Fingerprint

Vascular Calcification
Inflammation
Chronic Renal Insufficiency
alpha-2-HS-Glycoprotein
Tunica Intima
Inflammation Mediators
Serum
Osteoblasts
Vascular Smooth Muscle
C-Reactive Protein
Smooth Muscle Myocytes
Minerals
Dialysis
Coronary Vessels
Arteries
Cytokines
Morbidity
Mortality
Population

Keywords

  • Advanced glycation end products
  • C-reactive protein
  • Chronic kidney disease
  • Cytokines
  • Fetuin-A
  • Inflammation
  • Oxidation
  • Vascular calcification

ASJC Scopus subject areas

  • Nephrology
  • Hematology

Cite this

Inflammation and vascular calcification. / Moe, Sharon; Chen, Xuening (Neal).

In: Blood Purification, Vol. 23, No. 1, 2005, p. 64-71.

Research output: Contribution to journalArticle

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