In individuals without CKD, serum phosphate levels undergo marked diurnal variations, with peaks in the afternoon and early morning hours [79]. Surprisingly, dietary phosphate intake has a relatively modest effect on morning fasting serum phosphate levels in individuals with normal renal function, presumably as a result of hormonal regulatory mechanisms that modulate renal phosphate retention [12,79,80]. However, the chronic effect of two dietsdproviding 2300 and 625 mg phosphorus daily, respectively, but otherwise identicaldon diurnal phosphate levels was studied [79]. Diurnal phosphate levels were 12% lower on the low-phosphate diet, the afternoon phosphate levels were
35% lower, and calcitriol levels were 58% higher. Moreover, a clinical study cited above showed that a high-phosphate meal, but not a low-phosphate meal, could exert an acute adverse effect on endothelial function [69]. And, not surprisingly, a number of clinical studies have shown that an increase in dietary phosphate can provoke a compensatory increase in plasma FGF23dlikely explaining why increased dietary phosphate does not readily raise fasting serum phosphate levels [80–84]. More- over, calorie-corrected dietary phosphate intake correlates positively with plasma FGF23 in the HPFS (Health Professionals Follow-Up Study) trial; the increase was monotonic across quartiles of dietary phosphate [85]. Analogously, some although not all clinical studies find that increased phosphate intake in- creases PTH levels, and a cross-sectional study has correlated higher habitual phosphate intakes with higher PTH [