This study is aimed to review current knowledge about the influence of energy intake on mineral metabolism focussing on four aspects of major interest for the chronic kidney disease-metabolic bone disease (CKD-MBD) patient: (a) phosphate (P) handling, (b) fibroblast growth factor 23 (FGF23) and calcitriol synthesis and secretion, (c) metabolic bone disease, and (d) vascular calcification (VC). High caloric intake promotes P retention, while caloric restriction decreases plasma P concentrations. A direct correlation between energy intake and FGF23 has been shown in animals and humans while plasma calcitriol concentrations are inversely proportional to caloric intake. The effect of energy intake on bone is controversial. High caloric intake has been reported to increase bone mass, but the associated changes in adipokines and cytokines may as well be deleterious for bone. Low caloric intake tends to reduce bone mass but also may provide indirect beneficial effects on bone. Finally, while VC has been shown to be exacerbated by diets with high energy content, the opposite has not been demonstrated with low calorie intake. In conclusion, although prospective studies in humans are needed, when planning caloric intake for a CKD-MBD patient, it is important to take into consideration the associated changes in mineral metabolism.