In the course of chronic kidney disease (CKD), alterations in the bone-vascular axis augment the risk of bone loss, fractures, vascular and soft tissue calcification, left ventricular hypertrophy, renal and myocardial fibrosis, which markedly increase morbidity and mortality rates. A major challenge to improve skeletal and cardiovascular outcomes in CKD patients requires a better understanding of the increasing complex interactions among the main modulators of the bone-vascular axis. Serum parathyroid hormone (PTH), phosphorus (P), calcium (Ca), fibroblast growth factor 23 (FGF23), calcidiol, calcitriol and Klotho are involved in this axis interact with RANK/RANKL/OPG system and the Wnt/β-catenin pathway. The RANK/RANKL/OPG system controls bone remodeling by inducing osteoblast synthesis of RANKL and downregulating OPG production and it is also implicated in vascular calcification. The complexity of this system has recently increased due the discovery of LGR4, a novel RANKL receptor involved in bone formation, but possibly also in vascular calcification. The Wnt/β-catenin pathway plays a key role in bone formation: when this pathway is activated, bone is formed, but when it is inhibited, bone formation is stopped. In the progression of CKD, a downregulation of the Wnt/β-catenin pathway has been described which occurs mainly through the not coincident elevations of sclerostin, Dickkopf1 (Dkk1) and the secreted Frizzled Related Proteins (sFRPs). This review analyzes the interactions of PTH, P, Ca, FGF23, calcidiol, calcitriol and Klotho with the RANKL/RANKL/OPG system and the Wnt/β-catenin, pathway and their implications in bone and cardiovascular disorders in CKD.

在慢性肾病 (CKD) 病程中，骨-血管轴的改变会增加骨质流失、骨折、血管和软组织钙化、左心室肥厚、肾和心肌纤维化的风险，从而显着增加发病率和死亡率。改善 CKD 患者骨骼和心血管结局的主要挑战需要更好地了解骨 - 血管轴主要调节剂之间日益复杂的相互作用。血清甲状旁腺激素 (PTH)、磷 (P)、钙 (Ca)、成纤维细胞生长因子 23 (FGF23)、骨化二醇、骨化三醇和 Klotho 参与该轴与 RANK/RANKL/OPG 系统和 Wnt/β-连环蛋白相互作用途径。RANK/RANKL/OPG 系统通过诱导 RANKL 的成骨细胞合成和下调 OPG 的产生来控制骨重塑，并且它也与血管钙化有关。由于 LGR4 的发现，该系统的复杂性最近有所增加，LGR4 是一种参与骨形成但也可能参与血管钙化的新型 RANKL 受体。Wnt/β-catenin 通路在骨形成中起关键作用：当该通路被激活时，骨形成，但当它被抑制时，骨形成停止。在 CKD 的进展过程中，Wnt/β-catenin 通路的下调主要通过硬化蛋白、Dickkopf1 (Dkk1) 和分泌的卷曲相关蛋白 (sFRPs) 的不同程度升高而发生。本综述分析了 PTH、P、Ca、FGF23、骨化二醇、