Pathogenesis of renal osteodystrophy

Many major and minor factors have been involved in the pathogenesis of secondary hyperparathyroidism (SHP) of chronic renal failure (CRF). Among the major factors, phosphate retention, calcitriol and/or calcitriol-receptor deficiency, skeletal resistance to the calcemic action of PTH, and altered calcium-regulated PTH secretion have been claimed to play a predominant role. The present review mainly deals with the potential causal role of these factors in the initial events of SHF of CRF. A large amount of data confirm that phosphate retention, reduction in calcitriol-receptor availability, and bone resistance to PTH are very effective in determining the increase of PTH secretion in the course of CRF. However, a clear demonstration that any of these factors might play an initiating role is still lacking. As regards the hypothesized role for the altered calcium-regulated PTH secretion rate, no evidence exists of such an alteration, at least until the very late hypercalcemic form of SHP appears. In conclusion, none of the already known factors can be inequivocably considered as an initiating causal factor of SHP in CRF. As a consequence, in the absence of causal therapeutic intervention, care has to be taken during the correction of PTH hypersecretion, in order to avoid an oversuppression of parathyroid glands.