由于治疗学的进展,改善了肾功能衰竭患者的生存,因而使不易完全恢复的肾性骨营养不良等问题就显得更为重要。骨病通常为缓慢进行的肾功能衰竭的特征。它常常潜隐地发展,而仅在少数病人引起症状。晚期骨营养不良的治疗比较困难,而早期处理的指征又不很明确。如使用强有力的治疗药物则问题更为复杂,使用不当,可引起高钙血症或转移性钙化。本文主要讨论透析治疗前的骨病。病理生理学肾功能衰竭时的骨病是由进行性高磷血症和维生素D代谢改变所引起的。由于肾小球滤过率(GFR)下降,血浆磷浓度趋于上升而钙浓度则趋于下降。这种内环境恒定的紊乱可通过甲状旁腺素(PTH)分泌增加来矫正,PTH通过减少肾小管的重吸收而降低血浆磷浓度。根据PTH的水平,还可能有钙从骨中动员出 Because of the advances in therapies that improve the survival of patients with renal failure, the problems of renal osteodystrophy, which is not easily recoverable, are even more important. Bone disease is usually characterized by a slow progression of renal failure. It often develops subtly, and only causes symptoms in a small number of patients. Treatment of advanced bone malnutrition is more difficult, but the indications for early treatment are not very clear. If the use of powerful therapeutic drugs then the problem is more complex, improper use, can cause hypercalcemia or metastatic calcification. This article focuses on pre-dialysis treatment of bone disease. Pathophysiology Kidney failure of bone disease is caused by progressive hyperphosphatemia and vitamin D metabolism. As the glomerular filtration rate (GFR) decreased, the plasma phosphorus concentration tends to rise and the calcium concentration tends to decline. This constant internal disturbance can be corrected by an increase in parathyroid hormone (PTH) secretion, and PTH decreases plasma phosphorus by reducing renal tubular reabsorption. Depending on the level of PTH, calcium may also be mobilized from the bone