Introduction
Abnormalities of mineral metabolism lead to the development of vascular calcification and aortic stiffness in Chronic Kidney Disease (CKD) patients that contributes to cardiovascular disease.1-3 Despite normal values of calcium and phosphorus in the CKD population, 40% of CKD patients not receiving dialysis display evidence of calcification on imaging.4, 5 Opportunities to reduce or slow the progression of vascular calcification in early stages of CKD should be explored to hinder the establishment of vascular calcification. Phosphate binders for the management of secondary hyperparathyroidism in CKD patients not receiving dialysis is mainly limited to the correction of hyperphosphatemia. Several studies have illustrated the development of inflammation and abnormal mineral metabolism prior to the development of frank hyperphosphatemia.6-8 The trade-off in the nephron hypothesis suggests that a high concentration of phosphate in the cortical distal nephron reduces the concentration of ionized calcium in that segment, and thereby necessitates increased parathyroid hormone to maintain normal calcium reabsorption and normocalcemia.9 As such, the relative normal serum phosphate provides limited value in determining the detrimental effects of phosphate exposure.10-12 In this study, the effects of sevelamer carbonate or calcium acetate were compared for their role on biomarkers indicative of vascular calcification, inflammation, and endothelial dysfunction in patients with CKD stages 3 and 4 without hyperphosphatemia.