Fukagawa Masafumi, Hamada Yasuhiro, Nakanishi Shohei, Tanaka Motoko
Division of Nephrology and Dialysis Center, Kobe University School of Medicine, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
J Bone Miner Metab. 2006;24(6):434-8. doi: 10.1007/s00774-006-0719-7.
The kidney plays an important role in the regulatory system for bone and mineral metabolism. In chronic kidney disease (CKD), various abnormalities, recently named CKD-mineral and bone disorder (CKD-MBD), may develop in this system. The optimal management of CKD-MBD should be achieved without increasing the risk of metastatic calcification, including that of blood vessels. Thus, it is quite important to identify severe cases of hyperparathyroidism refractory to medical therapy. The size of the parathyroid glands, serum levels of fibroblast growth factor (FGF)23, and, possibly, the overproduction of a novel form of parathyroid hormone (PTH), serve as useful markers for this purpose. Adynamic bone disease with low buffering capacity for calcium is another major cause of hypercalcemia in dialysis patients. Our recent studies suggest that indoxyl sulfate accumulated in uremic serum is responsible for the suppression of osteoblastic function. In order to maintain the bone quality in patients with CKD, bone changes due to aging, menopause, and malnutrition need to be considered by nephrolgists and non-nephrologists in collaboration.
肾脏在骨骼和矿物质代谢调节系统中发挥着重要作用。在慢性肾脏病(CKD)中,该系统可能会出现各种异常情况,最近被称为CKD-矿物质和骨异常(CKD-MBD)。CKD-MBD的最佳管理应在不增加转移性钙化风险(包括血管钙化风险)的情况下实现。因此,识别药物治疗难治的严重甲状旁腺功能亢进病例非常重要。甲状旁腺的大小、成纤维细胞生长因子(FGF)23的血清水平,以及可能的一种新型甲状旁腺激素(PTH)的过度产生,可作为这方面有用的标志物。钙缓冲能力低的动力缺失性骨病是透析患者高钙血症的另一个主要原因。我们最近的研究表明,尿毒症血清中积累的硫酸吲哚酚是成骨细胞功能受抑制的原因。为了维持CKD患者的骨质,肾病学家和非肾病学家需要合作考虑衰老、绝经和营养不良导致的骨变化。