Chronic kidney disease-mineral bone disorder (CKD-MBD) is a common complication of CKD. The therapeutic strategies for the treatment of CKD-MBD include phosphate binders, active vitamin D analogs and calcimimetics. The first class of drugs provided nephrologists with a range of phosphate binders that are able to decrease circulating phosphate and parathyroid hormone but involve some tolerability and safety issues. In the past 2 years, new phosphate binders have been launched and others are still under development. Serum phosphate increases only in the late stages of CKD but clinical abnormalities begin to occur earlier when multiple mechanisms try to compensate for the progressive reduced ability of the kidney to eliminate phosphorus with urine. Accordingly, starting phosphate binders when phosphatemia reaches values higher than normal may represent a late therapeutic approach. Serum phosphorus is not the ideal biomarker for the diagnosis and treatment of phosphate imbalance. This role could be better played by fibroblast growth factor 23, whose serum concentrations rise earlier in CKD. A more detailed knowledge of the mechanisms underlying CKD-MBD development will provide new therapeutic targets and then new perspectives for the treatment of phosphate imbalance in the future.
Keywords: chronic kidney disease-mineral bone disorder; fibroblast growth factor 23; phosphate; phosphate binders; vascular calcifications.