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小儿慢性肾脏病-矿物质和骨异常的治疗

Treatment of Pediatric Chronic Kidney Disease-Mineral and Bone Disorder.

作者信息

Hanudel Mark R, Salusky Isidro B

机构信息

Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.

Division of Pediatric Nephrology, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, MDCC A2-383, Los Angeles, CA, 90095-1752, USA.

出版信息

Curr Osteoporos Rep. 2017 Jun;15(3):198-206. doi: 10.1007/s11914-017-0365-0.

Abstract

PURPOSE OF REVIEW

In this paper, we review the pathogenesis and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD), especially as it relates to pediatric CKD patients.

RECENT FINDINGS

Disordered regulation of bone and mineral metabolism in CKD may result in fractures, skeletal deformities, and poor growth, which is especially relevant for pediatric CKD patients. Moreover, CKD-MBD may result in extra-skeletal calcification and cardiovascular morbidity. Early increases in fibroblast growth factor 23 (FGF23) levels play a key, primary role in CKD-MBD pathogenesis. Therapeutic approaches in pediatric CKD-MBD aim to minimize complications to the growing skeleton and prevent extra-skeletal calcifications, mainly by addressing hyperphosphatemia and secondary hyperparathyroidism. Ongoing clinical trials are focused on assessing the benefit of FGF23 reduction in CKD. CKD-MBD is a systemic disorder that has significant clinical implications. Treatment of CKD-MBD in children requires special consideration in order to maximize growth, optimize skeletal health, and prevent cardiovascular disease.

摘要

综述目的

在本文中,我们回顾慢性肾脏病-矿物质和骨异常(CKD-MBD)的发病机制及治疗,尤其涉及儿科CKD患者。

最新发现

CKD中骨和矿物质代谢调节紊乱可能导致骨折、骨骼畸形及生长发育不良,这对儿科CKD患者尤为重要。此外,CKD-MBD可能导致骨骼外钙化及心血管疾病。成纤维细胞生长因子23(FGF23)水平早期升高在CKD-MBD发病机制中起关键的主要作用。儿科CKD-MBD的治疗方法旨在尽量减少对生长中骨骼的并发症并预防骨骼外钙化,主要通过解决高磷血症和继发性甲状旁腺功能亢进。正在进行的临床试验聚焦于评估降低CKD中FGF23的益处。CKD-MBD是一种具有重大临床意义的全身性疾病。儿童CKD-MBD的治疗需要特别考虑,以实现生长最大化、优化骨骼健康并预防心血管疾病。

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本文引用的文献

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