Coburn J W, Hartenbower D L, Brickman A S
Am J Clin Nutr. 1976 Nov;29(11):1283-99. doi: 10.1093/ajcn/29.11.1283.
Many clinical similarities between renal osteodystrophy and nutritional rickets have suggested that a defect in either the metabolism or action of vitamin D exists in chronic renal failure. The discovery of the kidney as the organ that manufactures the active metabolite of vitamin D has provided direct evidence for a relationship between renal failure and altered vitamin D metabolism. Other observations suggest that an abnormality of vitamin D action could underlie both osteomalacia and osteitis fibrosa (secondary hyperparathyroidism) observed in patients with chronic renal failure. The administration of the active vitamin D analogs, 25(OH)D3, 1,25(OH)2D3, and lalpha(OH)D3, to uremic patients with symptomatic bone disease is capable of reversing many of the abnormalities of divalent ion metabolism. The widespread availability of these agents in the future may provide the clinician the means to correct or even prevent the serious bone disease that frequently complicates the course of chronic renal failure.
肾性骨营养不良与营养性佝偻病在临床上有许多相似之处,这表明慢性肾衰竭患者存在维生素D代谢或作用缺陷。肾脏作为制造维生素D活性代谢产物的器官这一发现,为肾衰竭与维生素D代谢改变之间的关系提供了直接证据。其他观察结果表明,维生素D作用异常可能是慢性肾衰竭患者出现骨软化症和纤维性骨炎(继发性甲状旁腺功能亢进)的基础。对有症状性骨病的尿毒症患者给予活性维生素D类似物25(OH)D3、1,25(OH)2D3和1α(OH)D3,能够逆转许多二价离子代谢异常。这些药物在未来的广泛应用可能为临床医生提供纠正甚至预防经常使慢性肾衰竭病程复杂化的严重骨病的手段。