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Effect of Phosphate Binders in Chronic Kidney Disease Unclear

Last Updated: July 20, 2012.

 

Linked to lower urinary, serum phosphorus, but promote progression of vascular calcification

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Although phosphate binders lower serum and urinary phosphorus and reduce progression of secondary hyperthyroidism, they also promote progression of vascular calcification, and consequently their safety and efficacy for patients with chronic kidney disease is unclear, according to a study published online July 19 in the Journal of the American Society of Nephrology.

FRIDAY, July 20 (HealthDay News) -- Although phosphate binders lower serum and urinary phosphorus and reduce progression of secondary hyperthyroidism, they also promote progression of vascular calcification, and consequently their safety and efficacy for patients with chronic kidney disease (CKD) is unclear, according to a study published online July 19 in the Journal of the American Society of Nephrology.

To assess the effects of phosphate binders in patients with CKD, Geoffrey A. Block, M.D., from Denver Nephrology, and colleagues randomly assigned 148 patients with estimated glomerular filtration rate of 20 to 45 ml/min/1.73 m² to receive calcium acetate, lanthanum carbonate, sevelamer carbonate, or placebo. The change in mean serum phosphorus from baseline to the average of that at months three, six, and nine was assessed.

The researchers found that, in both active therapy and placebo groups, there was a significant decrease in serum phosphorus, from a baseline mean of 4.2 mg/dL to 3.9 and 4.1 mg/dL, respectively. There was a 22 percent decrease in the mean 24-hour urine phosphorus with phosphate binders, but not placebo. In the active therapy group, median serum intact parathyroid hormone remained stable, while it increased significantly in the placebo group. Plasma C-terminal fibroblast growth factor 23 levels were not significantly affected by active therapy. Calcification of the coronary arteries and abdominal aorta was significantly increased with active therapy (median increases of 18.1 versus 0.6 percent [P = 0.05] and 15.4 versus 3.4 percent [P = 0.03], respectively).

"While we continue to believe that serum, or blood, phosphorus is a key component of the increased cardiovascular risk associated with kidney disease, our results suggest the use of the currently approved phosphate binding drugs does not result in substantial reductions in serum phosphorus and may be associated with harm in this population," Block said in a statement. "Future clinical trials should be conducted in all populations with adequate placebo controls and should address alternative or complementary methods to reduce serum phosphorus."

Pharmaceutical companies and companies providing kidney care contributed funding for the study; several authors disclosed financial ties to the biopharmaceutical industry.

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