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慢性肾脏病与骨质疏松症:评估与管理

Chronic kidney disease and osteoporosis: evaluation and management.

作者信息

Miller Paul D

机构信息

University of Colorado Health Sciences Center, Colorado Center for Bone Research , Lakewood, CO, USA.

出版信息

Bonekey Rep. 2014 Jun 25;3:542. doi: 10.1038/bonekey.2014.37. eCollection 2014.

Abstract

Fractures across the stages of chronic kidney disease (CKD) could be due to osteoporosis, some form of renal osteodystrophy defined by specific quantitative histomorphometry or chronic kidney disease-mineral and bone disorder (CKD-MBD). CKD-MBD is a systemic disease that links disorders of mineral and bone metabolism due to CKD to either one or all of the following: abnormalities of calcium, phosphorus, parathyroid hormone or vitamin D metabolism; abnormalities in bone turnover, mineralization, volume, linear growth or strength; or vascular or other soft-tissue calcification. Osteoporosis, as defined by The National Institutes of Health, may coexist with renal osteodystrophy or CKD-MBD. Differentiation among these disorders is required to manage correctly the correct disorder to reduce the risk of fractures. While the World Health Organization (WHO) BMD criteria for osteoporosis can be used in patients with stages 1-3 CKD, the disorders of bone turnover become so aberrant by stages 4 and 5 CKD that neither the WHO criteria nor the occurrence of a fragility fracture can be used for the diagnosis of osteoporosis. The diagnosis of osteoporosis in stages 4 and 5 CKD is one of the exclusion-excluding either renal osteodystrophy or CKD-MBD as the cause of low BMD or fragility fractures. Differentiations among the disorders of renal osteodystrophy, CKD-MBD or osteoporosis are dependent on the measurement of specific biochemical markers, including serum parathyroid hormone (PTH) and/or quantitative bone histomorphometry. Management of fractures in stages 1-3 CKD does not differ in persons with or without CKD with osteoporosis assuming there is no evidence for CKD-MBD, clinically suspected by elevated PTH, hyperphosphatemia or fibroblast growth factor 23 due to CKD. Treatment of fractures in persons with osteoporosis and stages 4 and 5 CKD is not evidence based, with the exception of post hoc analysis suggesting efficacy and safety of specific osteoporosis therapies (alendronate, risedronate and denosumab) in stage 4 CKD. This review also discusses how to diagnose and manage fragility fractures across the five stages of CKD.

摘要

慢性肾脏病(CKD)各阶段出现的骨折可能归因于骨质疏松症、某种由特定定量组织形态计量学定义的肾性骨营养不良形式或慢性肾脏病-矿物质和骨异常(CKD-MBD)。CKD-MBD是一种全身性疾病,它将CKD导致的矿物质和骨代谢紊乱与以下一种或全部情况联系起来:钙、磷、甲状旁腺激素或维生素D代谢异常;骨转换、矿化、体积、线性生长或强度异常;或血管或其他软组织钙化。美国国立卫生研究院定义的骨质疏松症可能与肾性骨营养不良或CKD-MBD同时存在。需要区分这些疾病,以便正确管理相应病症,降低骨折风险。虽然世界卫生组织(WHO)的骨质疏松症骨密度标准可用于1-3期CKD患者,但到CKD 4期和5期时,骨转换紊乱变得非常异常,以至于WHO标准和脆性骨折的发生情况都不能用于骨质疏松症的诊断。CKD 4期和5期骨质疏松症的诊断是一种排除性诊断——排除肾性骨营养不良或CKD-MBD作为低骨密度或脆性骨折的原因。肾性骨营养不良、CKD-MBD或骨质疏松症之间的区分取决于特定生化标志物的测量,包括血清甲状旁腺激素(PTH)和/或定量骨组织形态计量学。假设没有因CKD导致的PTH升高、高磷血症或成纤维细胞生长因子23引起的临床疑似CKD-MBD证据,1-3期CKD患者骨折的管理与患有或未患有骨质疏松症的非CKD患者并无不同。除了事后分析表明特定骨质疏松症治疗(阿仑膦酸盐、利塞膦酸盐和地诺单抗)在4期CKD中有疗效和安全性外,骨质疏松症患者及4期和5期CKD患者骨折的治疗尚无循证依据。本综述还讨论了如何诊断和管理CKD五个阶段的脆性骨折。

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