Phosphate binders in uraemia: pharmacodynamics, pharmacoeconomics, pharmacoethics

Open Access
Publisher Website
Google Scholar
Abstract
In the past nephrologists were aware that the hyperphosphataemia of advanced renal failure triggered hyperparathyroidism, but because only few patients die from skeletal problems, hyperphosphataemia was treated with benign neglect. The panorama has abruptly changed after evidence accrued suggesting that hyperphosphataemia has adverse cardiovascular consequences. In some observational studies [ 1], but not consistently in all [ 2], pre‐dialysis serum P concentrations >6.5 mg/dl were associated with a higher relative risk of cardiovascular death. Furthermore, with the availability of electronbeam‐CT, a high prevalence of vascular, particularly coronary, calcification was noted in dialysed patients, which was progressive with time [ 3, 4]. Furthermore, the group of London has shown that active wall stiffness is correlated to vascular calcification [ 5]. Vascular calcifications are presumably more than the result of passive precipitation of Ca and P, and under certain conditions vascular smooth muscle cells can even acquire, at least partially, an osteoblastic phenotype.