Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a systemic dysfunction of mineral and bone metabolism in patients with CKD. It results from abnormalities in calcium, phosphorous, parathyroid hormone and/or vitamin D metabolism as well as abnormalities in bone turnover, mineralization, volume, linear growth or strength, in addition to vascular or other soft tissue calcification [
24]. Phosphate retention plays a crucial role in the development of CKD-MBD and it also increases the risk of cardiovascular events and mortality in patients with CKD [
25,
26]. In the early stages of CKD serum phosphate levels are maintained in the normal range through phosphaturia induced by increase in parathyroid hormone actions and fibroblast growth factor-23 (FGF-23) production. However, as kidney disease progresses the compensatory rise in FGF-23 levels fails to sustain phosphate clearance sufficiently and hyperphosphatemia ensues. Notably, increased FGF-23 levels by itself has been associated with increases in both cardiovascular events and mortality [
27,
28], suggesting that control of phosphate homeostasis early in CKD may help reducing the clinical consequences of mineral and bone disorders. Strategies to manage elevated serum phosphorus levels include reduction of dietary phosphate intake, as well as the use of phosphate binding agents. Clinical studies have assessed the effects of dietary phosphate and protein restriction in CKD patients. For example, patients with advanced CKD (stages 4 and 5) who had a reduction in dietary phosphates and protein intake also had improved short-term control of secondary hyperparathyroidism [
29‐
32]. In the long term, altering the diet allowed some patients to achieve a normal rate of bone formation [
33]. Recent evidence suggests that in addition to the absolute amount of phosphate in the diet, its source (i.e., plant
versus animal food) should be considered [
34]. Indeed, dietary phosphates from plant-derived proteins are mostly in the form of phytates, which are less digestible in humans. Consequently, phosphates are ultimately less bioavailable compared to phosphates derived from animal sources [
34]. Moe et al
. addressed this issue in nine patients who had established CKD (mean eGFR 32 mL/min/1.73 m
2) by comparing their responses to vegetarian- or meat-based diets with equivalent contents of protein and phosphates. After one week of the dietary intervention in their crossover study, the vegetarian diet led to lower serum levels of phosphorus and FGF-23 than the meat-based diet [
35]. Moreover, 13 patients with stages 3–5 CKD converted their food choices from an animal protein-based diet to a 70 % plant-protein diet for four weeks. The result was a significant reduction of urinary phosphorous excretion [
36] even though there were no significant changes in serum phosphorous or FGF-23 levels. The urinary sodium and titratable acid contents significantly decreased with the change to plant-based foods [
36]
. Overall, the combination of phosphate-restricted diets plus oral phosphate binders has become a well established approach to controlling serum phosphorus levels in patients with CKD stages 3–5 (including CKD stage 5D) [
24]. For example, a randomized controlled trial showed that dual intervention with a low-phosphorous diet and the addition of phosphate binders was more effective than either approach alone in reducing serum FGF-23 concentrations in 39 patients with CKD stages 3–4 and normal serum phosphate levels [
37]. Taken together, the results we have discussed suggest that restriction of dietary phosphate intake may improve the control of mineral and bone metabolism in CKD patients. Nevertheless, the prescription of low phosphate diets can be challenging in that the bioavailability of phosphates in foods (see above) needs to be considered.