Treatment of secondary hyperparathyroidism of predialysis chronic renal failure with low doses of 1,25(OH)2D3: humoral and histomorphometric results.
Treatment of secondary hyperparathyroidism of predialysis chronic renal failure with low doses of 1,25(OH)2D3: humoral and histomorphometric results.
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用低剂量 1,25(OH)2D3 治疗透析前慢性肾功能衰竭的继发性甲状旁腺功能亢进：体液和组织形态学结果。
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发表时间：
1986
期刊：
影响因子：
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通讯作者：
G. Cinotti
中科院分区：
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作者：
G. Coen;S. Mazzaferro;E. Bonucci;P. Ballanti;C. Massimetti;G. Donato;A. Landi;A. Smacchi;C. Della Rocca;G. Cinotti
一些作者主张用 1,25(OH)2D3 治疗继发性甲状旁腺功能亢进症和透析前慢性肾衰竭 (CRF) 的骨营养不良，但也因所谓的肾毒性而受到其他人的反对。然而，目前关于透析前CRF早期发生继发性甲状旁腺功能亢进症发病机制的概念表明，1,25(OH)2D3缺乏是主要因素。本研究的目的是评估以不会诱发高钙血症的剂量施用 1,25(OH)2D3（每天 0.25 微克）是否会改善透析前 CRF 的体液和骨组织形态学参数。 15 名透析前 CRF 患者（平均年龄 51.2 +/- 16.9 岁，范围 13-73 岁），血清肌酐 4.93 +/- 1.7 mg/dl，接受维生素 D 代谢物治疗平均 16.2 +/- 11.3 个月，最后进行经髂骨活检以进行组织形态测定。此外，23 名年龄、血清肌酐和肾衰竭原因具有可比性的患者作为对照。治疗不会引起高钙血症，也不会不利地改变肾功能下降的速度。碱性磷酸酶显着下降，而免疫反应性甲状旁腺激素 (iPTH) 和骨钙素则出现中度但不显着的下降。与对照患者相比，骨组织形态学参数主动吸收表面和主动成骨细胞表面显着降低，并且通过治疗几乎正常化。总之，该研究提供了确凿的证据，证明该代谢物在低剂量下不存在毒性，并且对骨组织学有良好的治疗反应。该剂量的治疗可在透析前 CRF 的早期阶段进行，无需密切、连续监测血清生化参数。
Treatment of secondary hyperparathyroidism and the osteodystrophy of predialysis chronic renal failure (CRF) with 1,25(OH)2D3 has been advocated by several authors, but also opposed by others for alleged renal toxicity. However, current concepts of the pathogenesis of the early occurrence of secondary hyperparathyroidism in predialysis CRF point to deficiency of 1,25(OH)2D3 as a primary factor. The aim of this study was to evaluate if administration of 1,25(OH)2D3 (0.25 microgram daily) in a dose which would not induce hypercalcemia, would improve humoral and bone histomorphometric parameters in predialysis CRF. 15 patients with predialysis CRF (mean age 51.2 +/- 16.9 years, range 13-73 years), serum creatinine 4.93 +/- 1.7 mg/dl, were treated with the vitamin D metabolite for an average of 16.2 +/- 11.3 months, at the end of which a transiliac bone biopsy for histomorphometry was performed. In addition, 23 patients comparable for age, serum creatinine and causes of renal failure, served as controls. Treatment did not induce hypercalcemia nor adversely modify the rate of decline of renal function. Alkaline phosphatase fell significantly while immunoreactive parathyroid hormone (iPTH) and osteocalcin showed a moderate, not significant, decrease. Compared to the control patients, the bone histomorphometric parameters active resorption surface and active osteoblastic surface were significantly lower and almost normalized by treatment. In conclusion, the study provides conclusive evidence of the absence of toxicity of the metabolite at the low doses employed, together with good therapeutic response on bone histology. Treatment at this dosage could be made in the early stages of predialysis CRF without need of close and continuous monitoring of serum biochemical parameters.