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.