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Perit Dial Int 27(Supplement_2): 215-222
2007
© 2007 International Society for Peritoneal Dialysis
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Part 6: Cardiovascular Complications in PD

AN OVERVIEW OF THE PATHOPHYSIOLOGY OF VASCULAR CALCIFICATION IN CHRONIC KIDNEY DISEASE

Tomasz Stompór

Chair and Department of Nephrology, Medical Faculty, Jagiellonian University, Cracow, Poland

Correspondence to: T. Stompór, Chair and Department of Nephrology, Medical Faculty, Jagiellonian University, 15c Kopernika Str., Cracow 31-501 Poland. stompin{at}mp.pl

Abnormalities of calcium–phosphate balance, with subsequent bone metabolism disorders, are among the key and earliest features of chronic kidney disease (CKD). Recently, another consequence of these abnormalities was brought to light—namely, vascular calcification. Most studies performed in patients on dialysis suggest that their vascular calcification is more advanced than that seen in the general population. Furthermore, the progression of vessel wall mineralization is much more dynamic in patients with CKD.

Apart from the commonly assessed factors that promote vascular calcification, such as age, duration of dialysis, or poor control of calcium–phosphate status, several other factors have recently been identified. In the spectrum of substances involved in the regulation of the process of soft-tissue calcification, the most extensively studied in the nephrology literature are bone morphogenetic protein 7, osteoprotegerin, matrix Gla protein, fetuin-A, and the phosphatonins. Better understanding of the mechanisms underlying excess vascular mineralization have led to the development of promising new therapies.

KEY WORDS: Chronic kidney disease; vascular calcification; calcification score; fetuin-A; osteoprotegerin; bone morphogenetic protein 7; phosphatonins; sevelamer; calcimimetics.




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