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慢性肾脏病患者骨质疏松症的管理。

Management of osteoporosis in patients with chronic kidney disease.

机构信息

Mansoura Nephrology and Dialysis Unit, Mansoura University, Mansoura, Egypt.

Division of Nephrology, Bone and Mineral Metabolism, University of Kentucky, 800 Rose Street, Room MN-560, Lexington, KY, 40536-0298, USA.

出版信息

Osteoporos Int. 2022 Nov;33(11):2259-2274. doi: 10.1007/s00198-022-06462-3. Epub 2022 Jun 24.

Abstract

Patients with CKD have a 4-fivefold higher rate of fractures. The incidence of fractures increases with deterioration of kidney function. The process of skeletal changes in CKD patients is characterized by compromised bone strength because of deterioration of bone quantity and/or quality. The fractures lead to a deleterious effect on the quality of life and higher mortality in patients with CKD. The pathogenesis of bone loss and fracture is complex and multi-factorial. Renal osteodystrophy, uremic milieu, drugs, and systemic diseases that lead to renal failure all contribute to bone damage in CKD patients. There is no consensus on the optimal diagnostic method of compromised bone assessment in patients with CKD. Bone quantity and mass can be assessed by dual-energy x-ray absorptiometry (DXA) or quantitative computed tomography (QCT). Bone quality on the other side can be assessed by non-invasive methods such as trabecular bone score (TBS), high-resolution bone imaging methods, and invasive bone biopsy. Bone turnover markers can reflect bone remodeling, but some of them are retained by kidneys. Understanding the mechanism of bone loss is pivotal in preventing fracture in patients with CKD. Several non-pharmacological and therapeutic interventions have been reported to improve bone health. Controlling laboratory abnormalities of CKD-MBD is crucial. Anti-resorptive therapies are effective in improving BMD and reducing fracture risk, but there are uncertainties about safety and efficacy especially in advanced CKD patients. Accepting the prevalent of low bone turnover in patients with advanced CKD, the osteo-anabolics are possibly promising. Parathyroidectomy should be considered a last resort for intractable cases of renal hyperparathyroidism. There is a wide unacceptable gap in osteoporosis management in patients with CKD. This article is focusing on the updated management of CKD-MBD and osteoporosis in CKD patients. Chronic kidney disease deteriorates bone quality and quantity. The mechanism of bone loss mainly determines pharmacological treatment. DXA and QCT provide information about bone quantity, but assessing bone quality, by TBS, high-resolution bone imaging, invasive bone biopsy, and bone turnover markers, can guide us about the mechanism of bone loss.

摘要

患有 CKD 的患者骨折发生率高出 4-5 倍。随着肾功能恶化,骨折的发生率会增加。CKD 患者骨骼变化的过程特征是由于骨量和/或质量恶化导致骨强度受损。骨折会对 CKD 患者的生活质量产生有害影响,并导致更高的死亡率。骨丢失和骨折的发病机制复杂且多因素。肾性骨营养不良、尿毒症环境、导致肾衰竭的药物和全身性疾病都会导致 CKD 患者的骨骼受损。目前,对于 CKD 患者的骨损伤评估的最佳诊断方法尚无共识。骨量和骨密度可以通过双能 X 线吸收法(DXA)或定量计算机断层扫描(QCT)进行评估。另一方面,骨质量可以通过非侵入性方法(如小梁骨评分(TBS)、高分辨率骨成像方法和侵入性骨活检)进行评估。骨转换标志物可以反映骨重塑,但其中一些被肾脏保留。了解骨丢失的机制对于预防 CKD 患者骨折至关重要。已经报道了几种非药物和治疗干预措施来改善骨骼健康。控制 CKD-MBD 的实验室异常至关重要。抗吸收疗法可有效改善 BMD 和降低骨折风险,但在 ADVANCED CKD 患者中,安全性和疗效存在不确定性。鉴于 ADVANCED CKD 患者普遍存在低骨转换,骨合成剂可能有希望。甲状旁腺切除术应被视为治疗难治性肾性甲状旁腺功能亢进的最后手段。在 CKD 患者的骨质疏松症管理中存在广泛的不可接受的差距。本文重点关注 CKD-MBD 和 CKD 患者骨质疏松症的最新管理。慢性肾脏病会降低骨质量和数量。骨丢失的机制主要决定药物治疗。DXA 和 QCT 提供骨量信息,但通过 TBS、高分辨率骨成像、侵入性骨活检和骨转换标志物评估骨质量,可以指导我们了解骨丢失的机制。

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