Pathophysiological mechanisms of vascular calcification in end-stage renal disease

M. R. Davies, K. A. Hruska

Research output: Contribution to journalComment/debate

205 Scopus citations

Abstract

Vascular calcification has been clearly defined as a risk factor for cardiovascular mortality in the general population and is highly prevalent in end-stage renal disease (ESRD), where it is associated with a number of markers of increased mortality such as left ventricular hypertrophy. The pattern of calcification in ESRD is characterized by mineral deposition in the tunica media, in contrast to non-ESRD populations, where calcification of atheromatous plaque predominates. This difference may have important clinical implications. The pathophysiological mechanisms underlying both types of vascular calcification remain to be clarified; however, current evidence suggests that they are active processes rather than passive mineral precipitation, and the presence in the vasculature of cells expressing an osteoblastic phenotype may be of central importance. In ESRD, the presence of secondary and tertiary hyperparathyroidism, disordered calcium and phosphate homeostasis, and the use of vitamin D- and calcium-based treatments in its therapy may all contribute to vascular calcification. These issues and the impact on other current and future therapies have great importance for clinical nephrology, and a better understanding of vascular calcification through a focused research effort is essential.

Original languageEnglish
Pages (from-to)472-479
Number of pages8
JournalKidney International
Volume60
Issue number2
DOIs
StatePublished - 2001

Keywords

  • Atheromatous plaque
  • Hyperparathyroidism
  • Left ventricular hypertrophy
  • Medial vascular calcification
  • Mineral deposition
  • Osteoblast-like cell
  • Renal osteodystrophy

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