Inflammation and vascular calcification

Research output: Contribution to journalReview article

82 Scopus citations

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 (US)
Pages (from-to)64-71
Number of pages8
JournalBlood Purification
Volume23
Issue number1
DOIs
StatePublished - Jan 20 2005

Keywords

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

ASJC Scopus subject areas

  • Nephrology
  • Hematology

Fingerprint Dive into the research topics of 'Inflammation and vascular calcification'. Together they form a unique fingerprint.

  • Cite this