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Clin Kidney J. 2016 Apr;9(2):280-6. doi: 10.1093/ckj/sfv145. Epub 2016 Jan 18.

Calcifying circulating cells: an uncharted area in the setting of vascular calcification in CKD patients.

Clinical kidney journal

Giuseppe Cianciolo, Irene Capelli, Maria Cappuccilli, Roberto Schillaci, Mario Cozzolino, Gaetano La Manna

Affiliations

  1. Nephrology, Dialysis and Renal Transplant Unit, S. Orsola Hospital, Department of Experimental Diagnostic and Specialty Medicine (DIMES) , University of Bologna , Bologna , Italy.
  2. Nephrology and Dialysis, S. Paolo Hospital, Department of Health Sciences (DISS) , University of Milan , Milan , Italy.

PMID: 26985381 PMCID: PMC4792620 DOI: 10.1093/ckj/sfv145

Abstract

Vascular calcification, occurring during late-stage vascular and valvular disease, is highly associated with chronic kidney disease-mineral and bone disorders (CKD-MBD), representing a major risk factor for cardiovascular morbidity and mortality. The hallmark of vascular calcification, which involves both media and intima, is represented by the activation of cells committed to an osteogenic programme. Several studies have analysed the role of circulating calcifying cells (CCCs) in vascular calcification. CCCs are bone marrow (BM)-derived cells with an osteogenic phenotype, participating in intima calcification processes and defined by osteocalcin and bone alkaline phosphatase expression. The identification of CCCs in diabetes and atherosclerosis is the most recent, intriguing and yet uncharted chapter in the scenario of the bone-vascular axis. Whether osteogenic shift occurs in the BM, the bloodstream or both, is not known, and also the factors promoting CCC formation have not been identified. However, it is possible to recognize a common pathogenic commitment of inflammation in atherosclerosis and diabetes, in which metabolic control may also have a role. Currently available studies in patients without CKD did not find an association of CCCs with markers of bone metabolism. Preliminary data on CKD patients indicate an implication of mineral bone disease in vascular calcification, as a consequence of functional and anatomic integrity interruption of BM niches. Given the pivotal role that parathyroid hormone and osteoblasts play in regulating expansion, mobilization and homing of haematopoietic stem/progenitors cells, CKD-MBD could promote CCC formation.

Keywords: atherosclerosis; calcifying circulating cells; chronic kidney disease-mineral and bone disorders; mineral metabolism; vascular calcification

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