Vascular Calcification in Chronic Kidney Disease: An Update

Mario Cozzolino,1 Francesco Cosa,2 Paola Ciceri,3 Francesca Elli,4 Flavia Ricca,5 Laura Cappelletti,5 Antonio Bellasi,4 Daniele Cusi6

1. Assistant Professor in Nephrology, Director of Laboratory of Experimental Nephrology, Department of Health Sciences, Renal Division, San Paolo Hospital, University of Milan, Italy
2. Renal Fellow, Department of Health Sciences, Renal Division, San Paolo Hospital, University of Milan, Italy
3. Laboratory of Experimental Nephrology, Department of Health Sciences, Renal Division, San Paolo Hospital, University of Milan, Italy
4. PhD, Student Laboratory of Experimental Nephrology, Department of Health Sciences, Renal Division, San Paolo Hospital, University of Milan, Italy
5. Student, Department of Health Sciences, Renal Division, San Paolo Hospital, University of Milan, Italy
6. Full Professor in Nephrology, Chief of Renal Division, San Paolo Hospital, University of Milan, Italy

Disclosure: No potential conflict of interest.
Citation: EMJ Neph. 2013;1:46-51.

Abstract

Vascular calcification involves passive degeneration and an active process of arterial mineralisation, resembling osteogenesis. In chronic kidney disease, several proteins that physiologically control bone mineralisation, are also involved in the molecular and cellular mechanisms of the pathogenesis of vascular calcification. In fact, arterial cells grown in culture are induced to become osteogenic by inflammatory and atherogenic stimuli, such as high phosphate concentration. Mechanisms linking them must be considered in clinical decisions. Further understanding of processes causing vascular calcification may be considered for new therapeutic options for vascular disease in renal patients.

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