Hyperphosphataemia in renal failure: causes, consequences and current management.

Hyperphosphataemia is prevalent among chronic renal failure and dialysis patients. It is known to stimulate parathyroid hormone and suppress vitamin D3 production, thereby inducing hyperparathyroid bone disease. In addition, it may independently contribute to cardiac causes of death through increased myocardial calcification and enhanced vascular calcification. Hyperphosphataemia is also associated with cardiac microcirculatory abnormalities. Therefore, phosphate control is of prime importance. It is important to control phosphate levels early in the course of chronic renal failure in order to avoid and treat secondary hyperparathyroidism, and cardiovascular and soft tissue calcifications. Dietetic restrictions are often difficult to follow long term. Because of its large sphere of hydration and the complex kinetics of phosphate elimination, phosphate is not easily removed by dialysis. Long, slow dialysis may be effective, but this needs logistics and acceptance by patients. Thus, oral phosphate binders are generally required to control serum levels. None of the existing phosphate binding agents is truly satisfactory. Aluminium-containing agents are highly efficient but many clinicians have abandoned their use because of the potential toxicity. Despite of the wide use of calcium-containing agents, there was a link with hypercalcaemia and soft tissue calcifications. Novel phosphate binders in the form of polyallylamine hydrochloride, polyuronic acid derivatives and lanthanum carbonate appear promising. In this review, we discuss causes of hyperphosphataemia, pathological consequences and modalities of treatment.