Some propose using
phosphate binders in the CKD population given the association between higher levels of
phosphorus and mortality, but their safety and efficacy in this population are not well understood. Here, we aimed to determine the effects of
phosphate binders on parameters of
mineral metabolism and
vascular calcification among patients with moderate to advanced CKD. We randomly assigned 148 patients with estimated GFR=20-45 ml/min per 1.73 m(2) to
calcium acetate,
lanthanum carbonate,
sevelamer carbonate, or placebo. The primary endpoint was change in mean serum
phosphorus from baseline to the average of months 3, 6, and 9. Serum
phosphorus decreased from a baseline mean of 4.2 mg/dl in both active and placebo arms to 3.9 mg/dl with active
therapy and 4.1 mg/dl with placebo (P=0.03).
Phosphate binders, but not placebo, decreased mean 24-hour urine
phosphorus by 22%. Median serum intact
parathyroid hormone remained stable with active
therapy and increased with placebo (P=0.002). Active
therapy did not significantly affect plasma C-terminal
fibroblast growth factor 23 levels. Active
therapy did, however, significantly increase calcification of the coronary arteries and abdominal aorta (coronary: median increases of 18.1% versus 0.6%, P=0.05; abdominal aorta: median increases of 15.4% versus 3.4%, P=0.03). In conclusion,
phosphate binders significantly lower serum and urinary
phosphorus and attenuate progression of
secondary hyperparathyroidism among patients with CKD who have normal or near-normal levels of serum
phosphorus; however, they also promote the progression of
vascular calcification. The safety and efficacy of
phosphate binders in CKD remain uncertain.