Vascular and Valvular Calcification in Chronic Kidney Disease: Pathogenesis and Clinical Outcomes

Vascular and valvular calcification contribute to the high burden of cardiovascular disease in patients with chronic kidney disease (CKD). In patients with CKD, vascular and valvular calcification result from an increase in calcium deposition due to metabolism confluence of inhibitory regulation of calcium deposition, increased matrix metalloproteinases (MMP) concentration, chronic inflammation, and the effect of mechanical stress. Vascular calcification leads to narrowing and dysfunction of vessels resulting in coronary artery disease (CAD) and peripheral artery disease (PAD). Valvular calcification leads to mitral annular calcification resulting in mitral regurgitation and stenosis, and to aortic valve calcification resulting in aortic stenosis. No current treatment can regress vascular/valvular calcification, but controlling traditional and CKD specific risk factors (i.e., mineral metabolism) can slow disease progression. In patients with CAD and PAD, percutaneous or surgical reperfusion is possible but technically challenging. Similarly, for symptomatic aortic and mitral valve disease, percutaneous valve replacements have emerged as a treatment option. Though valvular calcification can increase the risk of complication during these procedures, it can also provide the necessary landmarks and surface area that allow for a percutaneous valve deployment. More evidence is needed to evaluate these treatment strategies in this high-risk population.