The modern strategies to prevent secondary HPT in CRF pa­tients give great relevance to vitamin D replacement therapy, which requires to take into account the stage of CRF, the un­derlying renal disorder, the levels of circulating PTH, the condi­tion of the bone, the vitamin D stores, the parameters of bone turnover and the values of calcium and phosphate in serum. The administration of 1,25(OH)₂D or its analogues is unavoid­able in dialysis patients when secondary HPT is often already established. Its association with 25(OH)D or ergocalciferol or cholecalciferol may be beneficial for the bones, if a deficit of vi­tamin D stores is present (serum levels of 25(OH)D below 20­30 ng/mL). Therapeutic use of 25(OH)D or ergocalciferol is in­dicated in earlier stages of CRF to support renal ^-hydroxy­lase activity. At these stages, low doses of 1,25(OH)₂D may al­so be employed to prevent HPT since they are not harmful for renal function. The dose of vitamin D metabolites should be titrated on serum concentrations of calcium and phosphate, to avoid an excessively high calcium-phosphate product, and on serum PTH concentrations, to avoid excessive PTH suppres­sion and an adynamic condition of the bone. The aim of vitamin D replacement therapy is to prevent HPT since the early stages of CRF, because parathyroid hyperpla­sia and osteodystrophy cannot be completely reverted once developed. The attention of nephrologists has largely focused on dialysis patients and, unfortunately, few studies have ana­lyzed the outcome of vitamin D therapy in non-uremic patients. Because of the lack of clinical studies in this population no guidelines are available on when to start vitamin D replace­ment therapy in CRF patients. Therefore, it is likely that HPT and osteodystrophy are undertreated in a significant proportion of CRF patients. We have tried to summarize the criteria pro­posed in the current literature: one common criteria is that vita­min D therapy should be considered when serum 25(OH)D concentration is below 30 ng/mL. Instead, we do not know when 1,25(OH)₂D can be safely prescribed to non-uremic pa­tients and whether there are additional benefits by its associa­tion with 25(OH)D or ergocalciferol.

On the other hand, vitamin D therapy is not without problems, the first of which being vascular calcification. Again, we should make every effort to prevent vascular calcification since the early stages of CRF, because calcification is a non-reversible lesion. The K/DOQI guidelines provide some criteria to mini­mize the risk of calcium phosphate precipitation in terms of tar­get serum concentration of calcium and phosphate. However, our methods to fight calcification are limited and even the calci­um-phosphate product provides insufficient information. The therapeutical strategies for secondary HPT are now chang­ing. The availability of 1,25(OH)₂D analogues warrants inhibi­tion of parathyroid glands with lower effect on calcium and phosphate levels, and perhaps reduces mortality of dialysis pa­tients. In the near future 1,25(OH)₂D analogues will be com­bined with a new drug, cinacalcet, that directly inhibits PTH se­cretion and parathyroid proliferation. Potentially, the associa­tion of cinacalcet with 1,25(OH)₂D or its analogues is very promising because of the opposite effects of the two drugs on plasma calcium levels.
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