nutrients Review The Importance of Phosphate Control in Chronic Kidney Disease Ken Tsuchiya 1,* and Taro Akihisa 2 1 Department of Blood Purification, Tokyo Women’s Medical University, Tokyo 162-8666, Japan 2 Department of Nephrology, Tokyo Women’s Medical University, Tokyo 162-8666, Japan;
[email protected] * Correspondence:
[email protected] Abstract: A series of problems including osteopathy, abnormal serum data, and vascular calcification associated with chronic kidney disease (CKD) are now collectively called CKD-mineral bone disease (CKD-MBD). The pathophysiology of CKD-MBD is becoming clear with the emerging of αKlotho, originally identified as a progeria-causing protein, and bone-derived phosphaturic fibroblast growth factor 23 (FGF23) as associated factors. Meanwhile, compared with calcium and parathyroid hor- mone, which have long been linked with CKD-MBD, phosphate is now attracting more attention because of its association with complications and outcomes. Incidentally, as the pivotal roles of FGF23 and αKlotho in phosphate metabolism have been unveiled, how phosphate metabolism and hyperphosphatemia are involved in CKD-MBD and how they can be clinically treated have become of great interest. Thus, the aim of this review is reconsider CKD-MBD from the viewpoint of phosphorus, its involvement in the pathophysiology, causing complications, therapeutic approach based on the clinical evidence, and clarifying the importance of phosphorus management. Keywords: CKD-MBD; FGF23; aKlotho; phosphate-binder Citation: Tsuchiya, K.; Akihisa, T. The Importance of Phosphate Control in Chronic Kidney Disease. Nutrients 2021, 13, 1670. https://doi.org/ 1. Introduction 10.3390/nu13051670 The series of changes that occur in renal dysfunction, including decreases in serum calcium levels due to impairment in vitamin D activation, hypersecretion of parathyroid Academic Editor: Pietro hormone (PTH; i.e., secondary hyperparathyroidism), bone decalcification, and weak Manuel Ferraro bones (osteomalacia), were collectively regarded as renal osteodystrophy.