Sevelamer, or more precisely ‘sevelamer hydrochloride’, is a weakly basic anion-exchange resin in the chloride form that was introduced in 1997 for the treatment of the hyperphosphataemia of patients with end-stage renal failure, usually those on long-term haemodialysis. The rationale for this therapy was that sevelamer would sequester phosphate within the gastrointestinal tract, so preventing its absorption and enhancing its faecal excretion. Over the succeeding years, large numbers of patients have been treated with sevelamer, and it has fulfilled expectations in helping to control the hyperphosphataemia of end-stage renal failure. However, it is only one of many anion-exchange resins that could be used for this purpose, some of which are currently available for clinical use and are much less costly than sevelamer. Theoretical considerations suggest that some of these other resins might be at least as efficient as sevelamer in sequestering phosphate in the gastrointestinal tract. Neither sevelamer, nor any of these other agents, has been submitted to a proper metabolic balance study to measure the amount of phosphate sequestered by the resin in the bowel, and without this information it is impossible to judge which is the ideal resin for this purpose.

To the Editor: Vascular calcification was the subject of a recent review article [1], the subtitle of which was: Does preventing bone disease cause arterial disease? The authors discuss the possible link between calcium intake and cardiovascular disease. This link may be particularly important in patients with renal failure, but mention was made to the fact that a similar relation may exist in patients not on dialysis [2]. We have studied plasma calcium and phosphorus in 110 patients with coronary atherosclerosis and relatively preserved renal function (plasma creatinine smaller than 2 mg/dL) that underwent coronary angiography after an acute coronary syndrome [3]. Coronary artery disease burden was significant correlated with plasma calcium, but not with plasma phosphorus. A possible cut-off level for plasma calcium at 2.20 mmol/L was established [3]. These results are at odds with a previous report that showed that plasma phosphorus, but not plasma calcium, had an independent positive association with the angiographic severity of coronary disease, in a cohort of 376 stable patients without known renal disease [4]. It is unclear if subclinical renal failure (a condition in which phosphorus and calcium metabolism is changed) may have existed in this latter cohort. Plasma calcium [3] or plasma phosphorus [4] may be correlated with the severity of coronary atherosclerotic disease in patients with relatively preserved renal function [3], or in patients without known renal disease [4]. This may indicate a need for a reassessment of calcium supplementation, not only in dialysis patients, but also in patients with preserved renal function.

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