Shah Aniruddh, Hashmi Muhammad F., Aeddula Narothama R.
SBHGMC DHULE, INDIA
National Health Service
In 2005, Moe et al coined the term chronic kidney disease–mineral and bone disorder (CKD-MBD) to describe a complex clinical syndrome encompassing disorders of calcium, phosphate, parathyroid hormone (PTH), vitamin D, and fibroblast growth factor-23 (FGF23) metabolism. These disruptions lead to alterations in bone morphology (renal osteodystrophy), vascular calcification, and cardiovascular death in patients with chronic kidney disease (CKD). These abnormalities can potentially lead to high mortality rates, mainly from cardiovascular complications. Since the term CKD-MBD was introduced, various clinical guidelines have been developed, recommending specific laboratory targets and management options to improve the morbidity and mortality associated with this systemic syndrome. CKD-MBD can be assessed through histomorphometry of bone biopsy. Derangements in serum levels of calcium, phosphorus, PTH, and vitamin D, along with their effects on bone turnover, mineralization, and extraskeletal calcifications, are significant aspects of this syndrome. Although most features appear when the glomerular filtration rate (GFR) falls below 40 mL/min, some elements, such as loss of Klotho (a transmembrane protein), increased FGF23 secretion, decreased bone synthesis rates, and vascular calcification, often occur before abnormal biochemical markers manifest. Compelling evidence indicates a causal relationship between these derangements and numerous adverse clinical outcomes, particularly increased fracture risk and cardiovascular mortality. This activity highlights notable discoveries regarding the pathogenesis of CKD-MBD, including insights into the roles of FGF23, Klotho, Wnt inhibitors, and activin A. Management strategies for CKD-MBD primarily focus on preventing adverse effects associated with secondary hyperparathyroidism. Thus, management of secondary hyperparathyroidism is guided by established surrogate markers of deranged mineral bone metabolism, such as serum calcium, phosphate, PTH, and 25-hydroxyvitamin D. Renal osteodystrophy, an aspect of CKD-MBD, represents alterations in bone morphology. Although bone biopsy is the gold standard for diagnosing and classifying it, this invasive procedure is rarely performed. Kidney Disease Improving Global Outcomes (KDIGO) recommends monitoring the serial trend of biochemical markers for ongoing management of renal osteodystrophy. Furthermore, the 2017 update no longer advises performing a bone biopsy before initiating these medications.
2005年，莫伊等人创造了“慢性肾脏病-矿物质和骨代谢紊乱”（CKD-MBD）这一术语，用于描述一种复杂的临床综合征，该综合征包括钙、磷、甲状旁腺激素（PTH）、维生素D和成纤维细胞生长因子-23（FGF23）代谢紊乱。这些紊乱会导致慢性肾脏病（CKD）患者的骨形态改变（肾性骨营养不良）、血管钙化和心血管死亡。这些异常可能导致高死亡率，主要源于心血管并发症。自CKD-MBD这一术语被提出以来，已制定了各种临床指南，推荐了特定的实验室指标和管理方案，以改善与这种全身性综合征相关的发病率和死亡率。CKD-MBD可通过骨活检的组织形态计量学进行评估。血清钙、磷、PTH和维生素D水平的紊乱，以及它们对骨转换、矿化和骨骼外钙化的影响，是该综合征的重要方面。虽然大多数特征在肾小球滤过率（GFR）降至40 mL/min以下时出现，但一些因素，如Klotho（一种跨膜蛋白）的丢失、FGF23分泌增加、骨合成率降低和血管钙化，往往在异常生化指标出现之前就已发生。有力证据表明，这些紊乱与众多不良临床结局之间存在因果关系，尤其是骨折风险增加和心血管死亡率升高。这项活动重点介绍了关于CKD-MBD发病机制的显著发现，包括对FGF23、Klotho、Wnt抑制剂和激活素A作用的深入了解。CKD-MBD的管理策略主要侧重于预防与继发性甲状旁腺功能亢进相关的不良反应。因此，继发性甲状旁腺功能亢进的管理以矿物质骨代谢紊乱的既定替代指标为指导，如血清钙、磷、PTH和25-羟维生素D。肾性骨营养不良是CKD-MBD的一个方面，代表骨形态的改变。虽然骨活检是诊断和分类肾性骨营养不良的金标准，但这种侵入性操作很少进行。改善全球肾脏病预后组织（KDIGO）建议监测生化指标的连续趋势，以便对肾性骨营养不良进行持续管理。此外，2017年的更新不再建议在开始使用这些药物之前进行骨活检。
