Renal osteodystrophy and vascular calcification.

T. Arcidiacono, V. Paloschi, F. Rainone, A. Terranegra, E. Dogliotti, A. Aloia, L. Soldati, G. Vezzoli

Research output: Contribution to journalArticlepeer-review


Chronic kidney disease (CKD) is characterized by phosphate retention and reduced synthesis of 1.25(OH)2-vitamin D stimulating parathyroid hyperplasia. These changes cause a complex osteopathy, defined as renal osteodystrophy, and vascular calcification. Renal osteodystrophy increases the risk of fracture and causes deformities and disability. Vascular calcification occurs in a large proportion of hemodialysis patients and is a marker of arteriopathy. Calcifying arteriopathy induces arterial stiffness and contributes to the high cardiovascular mortality and morbidity among CKD patients. Vascular calcification results from a process of local bone formation induced by osteoblast-like cells developing in the vascular wall from resident cells. Osteoblast differentiation of resident vascular cells may be mediated by metabolic factors and may be induced by high concentrations of phosphate. Therefore, phosphate retention appears as the most detrimental factor affecting arteries in CKD patients. There is no specific therapy to revert soft tissue calcification, but calcification must be prevented in the early stages of CKD.

Original languageEnglish
Pages (from-to)21-26
Number of pages6
JournalJournal of Endocrinological Investigation
Issue number4 Suppl
Publication statusPublished - 2009

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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