慢性腎臟病患者相關的骨骼病變，稱為腎性骨病變(Renal Osteodystrophy)，其主要原因為鈣、磷、維生素D3、副甲狀腺素等代謝異常所致；而鈣、磷異常所導致的血管鈣化，正是造成長期透析病人死亡的主要原因。慢性腎衰竭的病人常因某些荷爾蒙異常所造成的骨骼變化如：副甲狀腺素分泌過多、活性維生素D3 [1,25(OH)2D3] (Calcitriol) 的不足或過量使用、Fibroblast Growth Factor 23(FGF-23) 的升高1。這些荷爾蒙異常中，續發性副甲狀腺的亢進和病人死亡率及罹病率有相當大的關係。目前臨床上，最常用於治療副甲狀腺亢進的藥物，為活性維生素D3 及鈣片；但使用活性維生素D3 後，易造成血鈣及血磷濃度上升，不但增加鈣化尿毒血管病變(Calciphylaxis) 的風險，並由於血磷上升，又再次促進副甲腺素分泌，如此會減低活性維生素D3 治療續發性副甲狀腺亢進的效果2。近年來，擬鈣劑(calcimimetics) 藥物的發明，除可有效抑制副甲狀腺素上升，亦可降低血鈣濃度，減緩血管鈣化。本文除探討慢性腎臟衰竭造成續發性副甲狀腺亢進的機轉和擬鈣劑的藥理作用機轉，並對副甲狀腺亢進的內外科處理方式，做進一步評估討論。

Renal osteodystrophy is a common bone problem for patients with chronic kidney disease. The most important reason for renal osteodystrophy is the imbalance of calcium,phosphate, vitamin D and parathyroid hormone. Blood vessel calcification, mostly made by high calcium and phosphate, is the major cause of death for long term dialysis patients. The bone disorder led by end stage chronic kidney disease is related to some hormone abnormal levels. For examples: the increase of parathyroid hormone, the decrease of D3 1,25(OH)2D3 (Calcitriol), and the increase of Fibroblast Growth Factor 23(FGF-23). These abnormal levels of hormones induce secondary hyperparathyroidism, which is the key of patients’ mortality and morbidity. Although in clinical, vitamin D and calcium are the usual medicines for hyperparathyroidism. Vitamin D, raising calcium and phosphate levels, brings the risk of vascular calcification or calciphylaxis. It is why large dose vitamin D lowers the outcome of treating secondary hyperparathyroidism. Calcimimetic agents, developed in recent years, succeed in control hyperparathyroidism, lessens calcium level, slows down blood vessel calcification and improves bone health in renal patients. This review article will discuss the varying effects of calcimimetic agents in renal medicine.