Calcium on trial: beyond a reasonable doubt?

To the Editor: Although the study by Chertow et al has shown that in hemodialysis patients, sevelamer compared to calcium-based phosphate binders is less likely to cause hypercalcemia and arterial calcifications, we do not think that in the patients of this study sevelamer should replace CaCO3. Indeed, their mild hyperparathyroidism could have been corrected by just higher doses of CaCO3 alone without aluminum hydroxide [Al (OH)3] or calcitriol. In fact, a high dose of CaCO3, without the co-administration of calcitrol, offers the distinct advantage of maintaining lower serum-phosphate concentration without higher serum calcium1. This is probably due to the fact that calcitriol increases intestinal absorption of phosphate whereas CaCO3 decreases it. Therefore, to clinically justify the preferential use of "sevelamer plus calcitriol" over that of CaCO3, the lower risk of arterial calcification should have been demonstrated against higher doses of CaCO3 without calcitriol while actually obtaining in both groups the same "targeted" ranges for serum concentrations of parathyroid hormone, calcium, and phosphate. The issue is indeed to know whether despite comparable serum chemistry, the higher oral doses of calcium are actually increasing the arterial calcium load more than calcitriol. However, the negative direct bone mineralization effect of calcitriol shown in vitamin D-receptor knockout mice2 does not support this possibility. The second issue is to know whether prevention of arterial calcification will improve cardiovascular risk independently of the improvement of uremic dyslipidemia, which promotes atherosclerosis and therefore intimal calcification. Indeed, the control of dyslipidemia with statin decreases cardiovascular morbid mortality in high-risk patients3 and is much cheaper than sevelamer as a cholesterol-lowering drug.