Seminars in Nephrology
Volume 24, Issue 5 , Pages 413-416, September 2004

Uremic vasculopathy

  • Sharon M. Moe

      Affiliations

    • Indiana University School of Medicine, Indianapolis, INUSA
    • Corresponding Author InformationAddress reprint requests to: Sharon M. Moe, MD, FACP, Associate Professor of Medicine, Associate Dean for Research Support, Indiana University School of Medicine, 1001 W. 10th St, OPW 526, Indianapolis, IN 46260

Recent evidence suggests that uremic vascular calcification is an active cell-mediated process resembling osteogenesis in bone rather than passive precipitation. We have identified increased expression of bone-associated proteins (osteopontin, bone sialoprotein, alkaline phosphatase, type I collagen), and the bone-specific transcription factor core-binding factor α-1 (Cbfa1) in histologic sections of inferior epigastric arteries obtained from patients with end-stage renal disease (ESRD) or calcific uremic arteriolopathy. In in vitro experiments, the addition of uremic serum to cultured vascular smooth muscle cells up-regulated osteopontin and Cbfa1 expression and accelerated mineralization. This implies that the uremic milieu may lead to dedifferentiation of vascular smooth muscle cells with subsequent mineralization. Further understanding of the pathophysiology of uremic vascular calcification is needed to design effective therapeutic strategies to intervene with this devastating condition in ESRD patients.

Keywords:  dialysis , vascular calcification , bone , calcific uremic arteriolopathy

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PII: S0270-9295(04)00098-1

doi:10.1016/j.semnephrol.2004.06.015

Seminars in Nephrology
Volume 24, Issue 5 , Pages 413-416, September 2004