In the early stages of
renal failure,
hyperparathyroidism develops as a compensatory mechanism to control serum levels of
calcium,
phosphorus and
calcitriol. As
kidney disease progresses, this ability to maintain
mineral homeostasis is lost, leading to the development of
renal osteodystrophy (ROD). Over the past decade, the pattern of ROD seen in patients with
chronic kidney disease (CKD) has changed. Previously, the majority of patients had mixed uraemic osteodystrophy or
aluminium-related
osteomalacia. The decreased use of
aluminium-based
phosphate binders, coupled with improvements in the management of hyperphosphataemia, led to a reduction in the prevalence of these types of ROD. Since the mid-1990s, there has been an increase in the prevalence of adynamic
bone disease as a result of increased suppression of
parathyroid hormone through the use of
calcium-based
phosphate binders and
calcitriol therapy. Adynamic
bone disease is also associated with several clinical factors, such as older age, use of
continuous ambulatory peritoneal dialysis and the presence of
diabetes mellitus, as well as the use of
calcitriol therapy. Studies of
calcium metabolism in patients with CKD have shown that adynamic
bone disease is a distinct clinical condition that leads to hypercalcaemia via mechanisms different from that seen in high-turnover bone disease. As high
calcium x
phosphorus product has been associated with soft tissue and
vascular calcifications, and increased mortality, optimizing bone health may be an important way of reducing cardiovascular risk in patients with CKD. To do this, novel, effective, non-
calcium, non-
aluminium phosphate binders will be necessary.