Vascular calcification in chronic kidney disease: an update

Georg Schlieper, Leon Schurgers, Vincent Brandenburg, Christiaan Reutelingsperger, Juergen Floege*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

149 Citations (Web of Science)

Abstract

Cardiovascular calcification is both a risk factor and contributor to morbidity and mortality. Patients with chronic kidney disease (and/or diabetes) exhibit accelerated calcification of the intima, media, heart valves and likely the myocardium as well as the rare condition of calcific uraemic arteriolopathy (calciphylaxis). Pathomechanistically, an imbalance of promoters (e.g. calcium and phosphate) and inhibitors (e.g. fetuin-A and matrix Gla protein) is central in the development of calcification. Next to biochemical and proteinacous alterations, cellular processes are also involved in the pathogenesis. Vascular smooth muscle cells undergo osteochondrogenesis, excrete vesicles and show signs of senescence. Therapeutically, measures to prevent the initiation of calcification by correcting the imbalance of promoters and inhibitors appear to be essential. In contrast to prevention, therapeutic regression of cardiovascular calcification in humans has been rarely reported. Measures to enhance secondary prevention in patients with established cardiovascular calcifications are currently being tested in clinical trials.
Original languageEnglish
Pages (from-to)31-39
JournalNephrology Dialysis Transplantation
Volume31
Issue number1
DOIs
Publication statusPublished - Jan 2016

Keywords

  • cardiovascular diseases
  • MGP
  • phenotype switch
  • vitamin K
  • VSMC

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