Osteodystrophy in the millennium

Despite three decades of intensive research on the derangements of calcium phosphate metabolism of renal failure, several unresolved issues are still with us at the turn of the millennium: poor control of hyperphosphatemia, r elative inefficacy of active vitamin D to prevent progressive parathyroid h yperplasia, and persistence of bone disease despite lowering of parathyroid hormone (PTH) and administration of active vitamin D. Although predictions are problematic, it is not unreasonable to hope that, barring unforeseen s ide effects, calcimimetics will prove to be valuable for suppressing or eve n preventing hyperparathyroidism, thus potentially replacing, at least in p art, active vitamin D. There is also reason to hope that more effective pho sphate binders with fewer side effects will become available and that contr olled studies will provide a rationale for the administration of estrogens to dialyzed women. As regards understanding the pathological mechanisms, on e can anticipate that the disturbances leading to autonomous growth of para thyroid cells will be elucidated and the signals involved in osteoclast/ost eoblast differentiation pathways and osteoclast/osteoblast coupling will be clarified, with obvious impact on patient management.