Pathophysiology of renal osteodystrophy

Pathophysiology of renal osteodystrophy
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肾性骨营养不良的病理生理学

DOI:
10.1007/s004670000341
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发表时间:
2000
影响因子:
3
通讯作者:
K. Hruska
K. Hruska
中科院分区:
医学3区
文献类型:
--
作者:
K. Hruska

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肾性骨营养不良是终末期肾病(ESRD)并发的骨骼疾病。它是一种多因素的骨重塑疾病。导致该疾病的一些因素是已知物质,其作用已明确,并且已设计出治疗方案来防止其影响。结果,肾性骨营养不良的性质发生了变化。例如,继发性甲状旁腺功能亢进症和 1α,25-二羟基胆钙化醇(骨化三醇)缺乏症被确定为肾性骨营养不良的主要诱因,从而导致了维持正常血清钙和磷酸盐浓度、减少甲状旁腺激素 (PTH) 分泌并纠正低骨化三醇水平的治疗。肾性骨营养不良治疗方面的这些改进导致纤维性骨炎的频率和严重程度降低,纤维性骨炎是肾性骨营养不良最常见和最重要的类型(表1)。从磷酸盐结合剂和透析用水中去除铝,减少了骨软化症和铝中毒的发生率,铝中毒是导致动力性骨病的原因(表 1)。与铝相关的骨病的发生率已经下降,但取而代之的是日益流行的无动力性骨病。由于这些进展,至少在初步基础上,已经产生并测试了与肾性骨营养不良发病机制相关的新假设。本文讨论了这些对骨骼生理学的新见解,并提出了建议未来研究和治疗方向的假设。纤维性骨炎的发病机制
Renal osteodystrophy is the skeletal disorder complicating end-stage renal disease (ESRD). It is a multifactorial disorder of bone remodelling. Some of the factors contributing to the disorder are known substances whose actions are well defined, and treatment regimens have been devised to prevent their effects. As a result, the nature of renal osteodystrophy has changed. For instance, the identification of secondary hyperparathyroidism and 1α,25-dihydroxycholecalciferol (calcitriol) deficiency as major contributors to renal osteodystrophy has led to treatment that maintains normal serum calcium and phosphate concentrations, reduces parathyroid hormone (PTH) secretion, and corrects low calcitriol levels. These improvements in the treatment of renal osteodystrophy have resulted in a decrease in the frequency and severity of osteitis fibrosa, the most-common and important type of renal osteodystrophy (Table 1). The removal of aluminum from the phosphate binders and the water used for dialysis has diminished the incidence of osteomalacia and aluminum intoxication as a cause of the adynamic bone disorder (Table 1). The frequency of aluminumrelated bone disease has waned only to be replaced by an increasing prevalence of the adynamic bone disorder. As a result of these developments new hypotheses related to the pathogenesis of renal osteodystrophy have been generated and tested, at least on a preliminary basis. These new insights into skeletal physiology are discussed here, and hypotheses are developed that suggest future directions for study and treatment. Pathogenesis of osteitis fibrosa
DOI: 10.1016/s0021-9258(18)61587-x
发表时间: 1987-02
期刊: The Journal of biological chemistry
影响因子: --
作者:
M. Centrella;T. McCarthy;E. Canalis
通讯作者: M. Centrella;T. McCarthy;E. Canalis
甲状旁腺激素抑制大鼠成骨肉瘤细胞中核糖核酸和蛋白质水平的胶原合成。
DOI: 10.1210/mend-3-2-232
发表时间: 1989
期刊: Molecular endocrinology (Baltimore, Md.)
影响因子: --
作者:
Partridge,NC;Dickson,CA;Kopp,K;Teitelbaum,SL;Crouch,EC;Kahn,AJ
通讯作者: Kahn,AJ