Bacchetta Justine, Bernardor Julie, Garnier Charlotte, Naud Corentin, Ranchin Bruno
Service de Néphrologie, Rhumatologie et Dermatologie Pédiatriques, Centre de Référence Des Maladies Rénales Rares, Centre de Référence Des Maladies Rares du Calcium et du Phosphore, Hôpital Femme Mère Enfant, Boulevard Pinel, 69677, Bron Cedex, France.
Université de Lyon, Lyon, France.
Calcif Tissue Int. 2021 Jan;108(1):116-127. doi: 10.1007/s00223-020-00665-8. Epub 2020 Jan 29.
Hyperphosphatemia is common in chronic kidney disease (CKD). Often seen as the "silent killer" because of its dramatic effect on vascular calcifications, hyperphosphatemia explains, at least partly, the onset of the complex mineral and bone disorders associated with CKD (CKD-MBD), together with hypocalcemia and decreased 1-25(OH) vitamin D levels. The impact of CKD-MBD may be immediate with abnormalities of bone and mineral metabolism with secondary hyperparathyroidism and increased FGF23 levels, or delayed with poor growth, bone deformities, fractures, and vascular calcifications, leading to increased morbidity and mortality. The global management of CKD-MBD has been detailed in international guidelines for adults and children, however, with difficulties to obtain an agreement on the ideal PTH targets. The clinical management of hyperphosphatemia is a daily challenge for nephrologists and pediatric nephrologists, notably because of the phosphate overload in occidental diets that is mainly due to the phosphate "hidden" in food additives. The management begins with a dietary restriction of phosphate intake, and is followed by the use of calcium-based and non-calcium-based phosphate binders, and/or the intensification of dialysis. The objective of this review is to provide an overview of the pathophysiology of hyperphosphatemia in CKD, with a focus on its deleterious effects and a description of the clinical management of hyperphosphatemia in a more global setting of CKD-MBD.
高磷血症在慢性肾脏病（CKD）中很常见。由于其对血管钙化有显著影响，常被视为“沉默的杀手”，高磷血症至少部分解释了与CKD相关的复杂矿物质和骨代谢紊乱（CKD-MBD）的发病机制，同时伴有低钙血症和1,25(OH)维生素D水平降低。CKD-MBD的影响可能是即时的，表现为骨和矿物质代谢异常、继发性甲状旁腺功能亢进和FGF23水平升高，也可能是延迟的，表现为生长发育不良、骨骼畸形、骨折和血管钙化，从而导致发病率和死亡率增加。国际成人和儿童指南已详细阐述了CKD-MBD的全球管理方法，然而，在理想的甲状旁腺激素（PTH）目标上难以达成共识。高磷血症的临床管理对肾脏病学家和儿科肾脏病学家来说是一项日常挑战，特别是因为西方饮食中的磷负荷过高，这主要是由于食品添加剂中“隐藏”的磷。管理首先从饮食中限制磷的摄入开始，然后使用钙基和非钙基磷结合剂，和/或加强透析。本综述的目的是概述CKD中高磷血症的病理生理学，重点关注其有害影响，并描述在更全面的CKD-MBD背景下高磷血症的临床管理。
