Abnormalities in
calcium and
phosphorus metabolism are common, and
metabolic bone disease develops often in patients with
chronic renal failure (CRF). Effective clinical management includes measures to control
phosphorus retention and prevent hyperphosphataemia, to maintain serum
calcium concentrations within the normal range and to prevent excess
parathyroid hormone (PTH) secretion by the judicious use of
vitamin D sterols. Certain of these interventions appear to increase the risk of soft tissue and
vascular calcification in patients with
end-stage renal disease (
ESRD), changes that may contribute to the development of
cardiovascular disease. Current therapeutic approaches are thus being re-evaluated in an effort to limit these risks. Despite the importance of controlling
phosphorus retention and preventing hyperphosphataemia in patients with CRF, current management strategies often are inadequate, particularly in those ingesting diets containing adequate amounts of
protein. Results from clinical trials using daily haemodialysis strongly suggest that thrice-weekly haemodialysis regimens are only marginally adequate for achieving weekly
phosphorus balance in many patients with
ESRD. The safety of large oral doses of
calcium as a
phosphate-binding agent in patients with
ESRD has also been questioned because excess amounts of
calcium that are absorbed from the gastrointestinal tract may lead to ongoing
calcium retention in those with little or no residual renal function. Arterial calcification and cardiac valve calcification are two serious complications that adversely affect cardiovascular haemodynamics. The use of large, often supraphysiological, doses of
calcitriol or other
vitamin D sterols to treat
secondary hyperparathyroidism may aggravate hypercalcaemia and hyperphosphataemia, further increasing the risk of soft tissue and
vascular calcification.
Phosphate-binding agents that do not contain
calcium, new
vitamin D analogues and calcimimetic compounds offer new therapeutic alternatives for managing
renal osteodystrophy. The integration of these novel agents into existing treatment regimens may provide safer and more effective methods for controlling
secondary hyperparathyroidism and renal
bone disease, while limiting the risks of soft tissue and
vascular calcification in patients with CRF.