The role of phosphorus in the genesis of azotemic osteodystrophy

There is good evidence for a role for phosphate retention in the genesis of secondary hyperparathyroidism. It exerts its effect directly by lowering the ionized calcium, thereby stimulating parathyroid secretion, and indirectly by causing skeletal resistance to the calcemic action of parathyroid hormone. The resistance phenomenon may be due in part to a direct effect of phosphorus on the skeletal resorbing action of parathyroid hormone and in part to an indirect effect of phosphorus on 1,25(OH)2D3 production. As well as causing parathyroid resistance, low serum 1,25(OH)2D3 is also responsible for decreased calcium absorption and may have a role in the mineralization disturbance seen in most cases of severe uremia. In the occasional instance, hypophosphatemia induced by phosphate-binding agents may contribute to uremic osteomalacia.