| [ Summary ] |
Vascular calcification is highly prevalent in hemodialysis patients compared to the general population. Vascular calcification is a progressive condition and is associated with arterial stiffness, as well as increased cardiovascular morbidity and mortality. The risk factors for vascular calcification in hemodialysis patients include age, duration of dialysis, diabetes mellitus, and hyperphosphatemia. The traditional view that vascular calcification is a degenerative and passive calcium deposition has been seriously challenged, based on strong evidence suggesting that vascular calcification is an active and highly regulated process similar to bone formation. In fact, some calcium regulatory proteins seem to be capable of inducing or inhibiting mineral deposition in vascular walls. In particular, bone morphogenetic protein 7, fetuin A, and matrix Gla protein may be regulatory keys in preventing vascular calcification in cases of uremia. Clinically, vascular calcification is detected through a number of techniques including plain radiographs, echocardiography, and CT scans. For prevention of vascular calcification in hemodialysis patients, reduction of serum phosphate levels is very important. Calcimimetics and calcium-free phosphate binders, such as sevelamer hydrochloride or lanthanum carbonate, provide new and effective therapeutic tools in preventing vascular calcification. This article presents the current understanding of the pathogenesis and prevention of vascular calcification in hemodialysis patients. |