Miller Paul D
University of Colorado Health Sciences Center, Colorado Center for Bone Research, Lakewood, CO 80227, USA.
Semin Nephrol. 2009 Mar;29(2):144-55. doi: 10.1016/j.semnephrol.2009.01.007.
Osteoporosis is the most prevalent metabolic bone disease leading to low-trauma (fragility) fractures worldwide. There is no reason why osteoporosis, as defined by different criteria, cannot accompany the derangements in bone metabolism that characterize chronic kidney disease (CKD). In fact, osteoporosis could and should be included in the broad characterization of CKD-mineral and bone disorder (CKD-MBD), as recently proposed by the Kidney Disease: Improving Global Outcomes working group. The pathophysiology leading to osteoporosis or CKD-MBD shares many common yet distinctly different pathways. Both pathways may lead to impairment of bone strength and low-trauma fractures. The challenge for clinical practice is how to discriminate between osteoporosis and CKD-MBD in fracturing patients. There is agreement that in the absence of aberrant biochemical tests suggesting CKD-MBD in stages 1 through 3 CKD, osteoporosis can be diagnosed using the World Health Organization criteria or development of low-trauma fractures. The distinction between osteoporosis and CKD-MBD becomes more difficult in stages 4 and 5 through 5D CKD. In fracturing patients with these levels of severe CKD, careful biochemical assessment of bone turnover markers and, in selected cases, bone biopsy is needed to eliminate CKD-MBD and to diagnose osteoporosis by exclusion. In stages 1 through 3 CKD, the current registered osteoporosis pharmacologic therapies can be used to treat osteoporosis. In stage 4, 5, and 5D these agents can be considered off-label, but only after very careful considerations and only in fracturing patients without CKD-MBD. We need better noninvasive means of discriminating among all these metabolic bone diseases and prospective data to guide us to the use of agents that alter bone remodeling in high-risk patients with more severe CKD.
骨质疏松症是全球最常见的代谢性骨病,可导致低创伤(脆性)骨折。根据不同标准定义的骨质疏松症,没有理由不能与慢性肾脏病(CKD)所特有的骨代谢紊乱同时存在。事实上,正如肾脏病:改善全球预后工作组最近所提议的,骨质疏松症可以而且应该纳入CKD-矿物质和骨异常(CKD-MBD)的广义范畴。导致骨质疏松症或CKD-MBD的病理生理学有许多共同但又明显不同的途径。这两种途径都可能导致骨强度受损和低创伤骨折。临床实践面临的挑战是如何在骨折患者中区分骨质疏松症和CKD-MBD。人们一致认为,在1至3期CKD患者中,若没有提示CKD-MBD的异常生化检查结果,则可使用世界卫生组织标准或低创伤骨折的发生情况来诊断骨质疏松症。在4期以及5至5D期CKD患者中,区分骨质疏松症和CKD-MBD变得更加困难。对于患有这些严重程度CKD的骨折患者,需要仔细进行骨转换标志物的生化评估,在某些情况下还需要进行骨活检,以排除CKD-MBD并通过排除法诊断骨质疏松症。在1至3期CKD患者中,目前已注册的骨质疏松症药物疗法可用于治疗骨质疏松症。在4期、5期和5D期,这些药物可被视为超说明书用药,但仅在经过非常仔细的考虑后,且仅用于没有CKD-MBD的骨折患者。我们需要更好的非侵入性方法来区分所有这些代谢性骨病,并需要前瞻性数据来指导我们在患有更严重CKD的高危患者中使用改变骨重塑的药物。