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Abstract
Patients with end-stage renal disease (ESRD) suffer from excess morbidity and mortality rates mostly due to cardiovascular disease. Both ‗traditional risk factors‘ and non-traditional uremia related risk factors lead to accelerated atherosclerosis and vascular calcification; and hence contributing the high prevalence of cardiovascular disease in those patients.
VC in particular has been of increasing interest within renal literature in the recent past. Two distinct but potentially co-localising forms of VC, intimal and medial calcification, have been identified. They appear to progress by a series of elaborate mechanisms similar to bony ossification and may involve genetic susceptibility or gene polymorphisms. A variety of proteins and tissue factors as well as soluble circulating molecules have been implicated in the pathogenesis of VC although the exact mechanisms remain to be unraveled.