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[慢性肾脏病中的磷代谢紊乱]

[Disturbance of phosphorus metabolism in chronic kidney disease].

作者信息

Komaba Hirotaka, Fukagawa Masafumi

机构信息

Kobe University School of Medicine, Division of Nephrology and Kidney Center.

出版信息

Clin Calcium. 2009 Feb;19(2):166-72.

Abstract

The kidney plays a central role in the maintenance of phosphorus homeostasis. Thus disturbance of phosphorus metabolism develops in most patients with chronic kidney disease (CKD) . Hyperphosphatemia typically occur in advanced CKD patients of whose glomerular filtration rate is <30 ml/min, whereas in early-stage CKD normophosphatemia is maintained by increased secretion of fibroblast growth factor-23 (FGF-23) and parathyroid hormone. Serum levels of these phosphaturic hormones increase along with the progression of CKD, leading to extremely high concentrations in dialysis patients, which in turn causes hypophosphatemia after kidney transplantation. Recently, besides phosphorus levels, increase in FGF-23 levels has been shown to predict mortality and progression of CKD. Further studies should investigate whether management of phosphorus balance in early-stage CKD is helpful in improving clinical outcomes and whether FGF-23 can be used as a potential biomarker for monitoring the response to its management.

摘要

肾脏在维持磷稳态中起核心作用。因此,大多数慢性肾脏病(CKD)患者会出现磷代谢紊乱。高磷血症通常发生在肾小球滤过率<30 ml/min的晚期CKD患者中,而在早期CKD患者中,通过成纤维细胞生长因子-23(FGF-23)和甲状旁腺激素分泌增加维持血磷正常。随着CKD的进展,这些排磷激素的血清水平升高,导致透析患者体内浓度极高,进而在肾移植后引起低磷血症。最近,除了磷水平外,FGF-23水平升高已被证明可预测CKD的死亡率和进展。进一步的研究应调查早期CKD患者磷平衡的管理是否有助于改善临床结局,以及FGF-23是否可作为监测其管理反应的潜在生物标志物。

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