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继发性甲状旁腺功能门进症(甲旁亢)几乎可发生于所有的慢性肾功能衰竭患者。磷酸盐潴留及高磷酸盐血症(高磷血症)在诱发和加重继发性甲旁亢以及引起骨骼外钙化方面起着举足轻重的作用。磷酸盐潴留引起甲旁亢的主要途径尚未彻底弄清。不过,已知高磷血症可借降低血钙而间接刺激甲状旁腺素释放。磷酸盐负荷还可减少肾脏合成的骨化三醇(12,25——二羟胆钙化醇),使甲状旁腺素释放增多。随着肾功能不全的进展而潴留磷酸盐但高磷血症在肾功能下降到正常的25％之前很少发生。肾衰
Secondary parathyroid gating (hyperparathyroidism) occurs in almost all patients with chronic renal failure. Phosphate retention and hyperphosphatemia (hyperphosphatemia) play an important role in inducing and exacerbating secondary hyperparathyroidism and in causing extracortical calcifications. Phosphate retention caused by hyperparathyroidism has not yet completely clear the main way. However, it is known that hyperphosphatemia indirectly stimulates parathyroid hormone release by lowering blood calcium. Phosphate load can also reduce the synthesis of calcitriol in the kidneys (12,25 - dihydroxycholecalciferol), parathyroid hormone release increased. Phosphates persist as renal insufficiency progresses but hyperphosphatemia rarely occurs until renal function drops to 25% of normal. Renal failure