Service of Pneumology, Hôpitaux Universitaires de Genève, Geneva, Switzerland.
Service of Nephrology, Hôpitaux Universitaires de Genève, Geneva, Switzerland.
Nephrology (Carlton). 2024 Dec;29(12):791-800. doi: 10.1111/nep.14407. Epub 2024 Oct 21.
Chronic kidney disease-mineral bone disorder (CKD-MBD) is a syndrome commonly observed in subjects with impaired renal function. Phosphate metabolism has been implicated in the pathogenesis of CKD-MBD and according to the phosphorocentric hypothesis may be the key player in the pathogenesis of these abnormalities. As phosphorous is an essential component for life, absorption from the bowel, accumulation and release from the bones, and elimination through the kidneys are all homeostatic mechanisms that maintain phosphate balance through very sophisticated feedback mechanisms, which comprise as main actors: vitamin D (VD), parathyroid hormone (PTH), calciproteins particles (CPPs), fibroblast growth factor-23 (FGF-23) and other phosphatonins and klotho. Indeed, as the renal function declines, factors such as FGF-23 and PTH prevent phosphate accumulation and hyperphosphatemia. However, these factors per se may be responsible for the organ damages associated with CKD-MBD, such as bone osteodystrophy and vascular calcification. We herein review the current understanding of the CKD-MBD focusing on phosphorous metabolism and the impact of phosphate manipulation on surrogate and hard outcomes.
慢性肾脏病-矿物质和骨异常（CKD-MBD）是肾功能受损患者中常见的综合征。磷代谢与 CKD-MBD 的发病机制有关，根据磷中心假说，磷可能是这些异常发病机制中的关键因素。由于磷是生命的必需成分，因此从肠道吸收、从骨骼中积累和释放以及通过肾脏排泄都是通过非常复杂的反馈机制来维持磷平衡的体内平衡机制，其中主要参与者包括：维生素 D（VD）、甲状旁腺激素（PTH）、钙磷蛋白颗粒（CPPs）、成纤维细胞生长因子 23（FGF-23）和其他磷调蛋白和 klotho。事实上，随着肾功能下降，FGF-23 和 PTH 等因素可防止磷的积累和高磷血症。然而，这些因素本身可能是与 CKD-MBD 相关的器官损伤的原因，例如骨营养不良和血管钙化。本文综述了 CKD-MBD 的当前认识，重点介绍了磷代谢以及磷干预对替代和硬终点的影响。
