Vascular calcification is a very common event in patients affected by diabetes and
chronic kidney disease (CKD). Recently, it has been well documented that abnormalities in mineral
and bone metabolism in CKD patients are associated with increased morbidity and mortality.
Elevated serum phosphate and calcium-phosphate product levels play an important role in
the pathogenesis of vascular mineralization in uremic patients and also appear to be associated
with increased cardiovascular mortality. Together with classical passive precipitation of calciumphosphate
in soft tissues, during the last decade it has been demonstrated that inorganic phosphate
may cause extraskeletal calcification directly through a real “ossification” of the tunica
media in the vasculature of CKD patients. Therefore, control of phosphate retention is now an
even more crucial target of treatment in patients affected by chronic kidney disease. (Heart International
2006; 2: 6-11)
