Aluminium- or
calcium-based
phosphate-binding agents traditionally have been used to treat hyperphosphataemia in patients with
end-stage renal disease. Although these agents effectively lower serum
phosphorus levels, they are associated with serious side effects.
Aluminium-based agents are associated with bone toxicity,
renal osteodystrophy and
encephalopathy, and
calcium-based agents increase the risk of hypercalcaemia and cardiovascular calcification. Consequently, there remains a need for new, safe and effective non-
calcium-, non-
aluminium-based alternative treatments. Fortunately, several new agents are now available or are in the late stages of development, including
sevelamer hydrochloride and
lanthanum carbonate. Although
sevelamer hydrochloride represents a step forward in the management of hyperphosphataemia, it has several drawbacks and is far from being the ideal
phosphate binder.
Lanthanum carbonate is the most recent non-
calcium, non-
aluminium phosphate binder to be developed for the treatment of hyperphosphataemia. Animal studies have shown it to be as effective as
aluminium, without the associated toxicity. In clinical studies,
lanthanum carbonate significantly reduced serum
phosphorus levels, compared with placebo. It shows a similar efficacy to
calcium carbonate in controlling serum
phosphorus levels, but requires lower doses. In addition,
lanthanum carbonate is at least as well tolerated as
calcium carbonate, but is not associated with hypercalcaemia. Importantly, it has a positive effect on bone histology, with no evolution towards low bone turnover.
Lanthanum carbonate, therefore, moves closer to the ideal
phosphate binder.