Mineral and Bone Disorders After Kidney Transplantation.

Mineral and Bone Disorders After Kidney Transplantation.
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DOI:
10.3389/fmed.2018.00211
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发表时间:
2018
影响因子:
3.9
通讯作者:
Ramanathan V
Ramanathan V
中科院分区:
医学3区
文献类型:
--
作者:
Vangala C;Pan J;Cotton RT;Ramanathan V

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慢性肾病患者发生矿物质和骨骼疾病的风险显著升高,主要是由于钙、磷、维生素D、甲状旁腺激素和成纤维细胞生长因子23的改变。这些矿物质和激素之间的交织关系导致适应不良反应,这些反应受到肾移植过程的不同影响。在移植后环境中,常规实验室、影像学和其他骨折风险评估工具的解释并不标准化。移植后骨疾病的改善并不一致,在监测和治疗实践中存在相当大的差异。在移植后阶段通常会遇到一系列异常,如低磷酸盐血症、高钙血症、高甲状旁腺激素、骨软化、骨质减少和骨质疏松症。因此,降低骨折风险和其他骨相关并发症需要认识到这些异常沿着使用免疫抑制剂所引起的风险。随着肾移植受者年龄的不断增长,在整个移植后期间,骨疾病的驱动因素在持续性甲状旁腺功能亢进、原发性甲状旁腺功能亢进和骨质疏松症之间变化。使用抗吸收疗法需要了解不同的选择和保证其使用的临床情况。由于强调骨折等临床事件的研究有限,需要专家对MBD生理学的理解和替代标记物的解释来确定理想的个性化治疗。
The risk of mineral and bone disorders among patients with chronic kidney disease is substantially elevated, owing largely to alterations in calcium, phosphorus, vitamin D, parathyroid hormone, and fibroblast growth factor 23. The interwoven relationship among these minerals and hormones results in maladaptive responses that are differentially affected by the process of kidney transplantation. Interpretation of conventional labs, imaging, and other fracture risk assessment tools are not standardized in the post-transplant setting. Post-transplant bone disease is not uniformly improved and considerable variation exists in monitoring and treatment practices. A spectrum of abnormalities such as hypophosphatemia, hypercalcemia, hyperparathyroidism, osteomalacia, osteopenia, and osteoporosis are commonly encountered in the post-transplant period. Thus, reducing fracture risk and other bone-related complications requires recognition of these abnormalities along with the risk incurred by concomitant immunosuppression use. As kidney transplant recipients continue to age, the drivers of bone disease vary throughout the post-transplant period among persistent hyperparathyroidism, de novo hyperparathyroidism, and osteoporosis. The use of anti-resorptive therapies require understanding of different options and the clinical scenarios that warrant their use. With limited studies underscoring clinical events such as fractures, expert understanding of MBD physiology, and surrogate marker interpretation is needed to determine ideal and individualized therapy.
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