Serum phosphate levels, along with serum calcium and parathyroid hormone (PTH), are the most commonly used markers for the diagnosis, monitoring and treatment of chronic kidney disease (CKD)-mineral and bone disorder (MBD) abnormalities in patients affected by kidney failure. Hyperphosphatemia appears late in the course of CKD, but the consequences of phosphate retention, such as increased levels of FGF23 and hyperparathyroidism, can be appreciated much earlier. Clinical practice guidelines suggest aiming at phosphate levels that currently are reached by no more than 50% of patients, despite major efforts of nephrologists, nurses and dieticians in addressing the issue of dietary and pharmacological compliance. Thus, there are margins of improvement of phosphate management in CKD patients, which could be accomplished by dietary and/or pharmacological approaches aimed at improving patient compliance. Severe hyperphosphatemia is always associated with phosphate overload, but it should be kept in mind that even mild hyperphosphatemia can be linked to a positive phosphate balance and its deleterious consequences. In fact, hyperphosphatemia is associated with mortality and morbidity (including hyperparathyroidism, left ventricular hypertrophy, and vascular calcifications). Management of hyperphosphatemia should take into account the main rings of the therapeutic chain of phosphate control: defense of residual renal function, adequate dialysis, diet, and phosphate binders. Along with the traditional approaches to phosphate control, in this article new aspects of phosphate control are summarized, such as cooking tips, education regarding the presence of phosphate-based additives/preservatives in foods and even drugs, and the potential advantages of last-generation phosphate binders.