Abstract
Vascular calcification is associated with the mortality of patients with chronic kidney disease (CKD) . Susceptibility to vascular calcification is genetically determined and actively regulated by diverse inducers and inhibitors. One of these inducers, hyperphosphatemia, promotes vascular calcification and is a nontraditional risk factor for CVD mortality in CKD patients. Hyperphosphatemia promotes vascular calcification in part by promoting VSMCs to undergo an osteochondrogenic phenotype change through a mechanism requiring sodium-dependent phosphate cotransporters. Recent randomized clinical trials showed that lowering serum phosphate levels with a non-calcium containing phosphate binder slows progression of vascular calcification in ESRD patients. Moreover, calcimimetics reduce arterial remodeling and calcification in rats with subtotal nephrectomy. Whether this difference will also be found in humans and will ultimately translate into less CV events in calcimimetics treated uremic patients is for a matter for speculation. Calcium and phosphate load are an important driver of vascular calcification.
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