Moorthy A V, Harrington A R, Mazess R B, Simpson D P
Clin Nephrol. 1981 Aug;16(2):93-100.
Patients with end-stage renal failure develop osteodystrophy in part due to defective production of 1,25-dihydroxycholecalciferol by the kidney. We treated eight adults with chronic renal failure and osteodystrophy with 1,25-dihydroxycholecalciferol (calcitriol) for 30-44 months. Seven of these patients were also symptomatic with bone pain and/or muscle weakness. Striking amelioration of muscle weakness occurred, and bone pain was considered to be significantly improved in four of seven patients. Hypercalcemia was noted in all the patients, necessitating a reduction in the daily dose of calcitriol to a range of 0.125 to 0.5 microgram/day. While serum alkaline phosphatase fell during therapy, serum iPTH did not show any significant change. Bone mineral content improved in four patients, though it still remained below normal. Radiographic changes of osteodystrophy showed definite improvement in only three.
终末期肾衰竭患者会出现骨营养不良,部分原因是肾脏产生1,25 - 二羟胆钙化醇存在缺陷。我们用1,25 - 二羟胆钙化醇(骨化三醇)对8名患有慢性肾衰竭和骨营养不良的成年人进行了30至44个月的治疗。其中7名患者还伴有骨痛和/或肌肉无力症状。肌肉无力症状显著改善,7名患者中有4名的骨痛被认为有明显改善。所有患者均出现高钙血症,因此需要将骨化三醇的每日剂量减至0.125至0.5微克/天的范围。治疗期间血清碱性磷酸酶下降,但血清iPTH没有明显变化。4名患者的骨矿物质含量有所改善,不过仍低于正常水平。骨营养不良的影像学改变仅在3名患者中显示出明确改善。