Diabetes Modifies Effect of High-Phosphate Diet on Fibroblast Growth Factor-23 in Chronic Kidney Disease

Context: The pathophysiology of calcium-phosphate disturbances in diabetic (DM) kidney disease differs from that in non-DM chronic kidney disease (CKD). Objective: We compared the effect of a 6-day high-phosphate diet on serum fibroblast growth factor-23 (FGF-23) and other parameters of calcium-phosphate metabolism in DM and non-DM CKD patients. Design and Setting: This was a prospective interventional study in a research center setting. Participants, Intervention, and Measures: Twenty-six nondialysis patients with stages 3-5 CKD and albuminuria less than 300 mg/g creatinine were recruited from February 2011 to November 2012 (15 DM, 11 non-DM). All patients received a high-phosphate diet (1800 mg/d) for 6 days. At baseline, day 3, and day 7 serum FGF-23, PTH, Ca, P, 25-hydroxyvitamin D, 1,25 dihydroxyvitamin D, monocyte chemoattractant protein-1, and calcium and phosphate urine excretion were measured. Results: In DM CKD patients, serum calcium was lower on days 3 and 7 vs baseline (P < .01, respectively), and innon-DM patients, it was unchanged. Serum phosphorus increased significantly only in non-DM patients on days 3 and 7 vs baseline (P < 0.01, respectively). Serum PTH was higher in the DM group on day 7 vs baseline (P = .04). Plasma 25-hydroxyvitamin D, 1,25 dihydroxyvitamin D, and serum monocyte chemoattractant protein-1 were unchanged in both groups. Serum FGF-23 increased in DM patients, from baseline to day 3 (58.1 +/- 52.7 and 91.6 +/- 71.1 pg/mL, P = .001) but later tended to decrease. In non-DM patients, there was a steady increase of FGF-23 between baseline and day 7 (75 +/- 84.3 to 176 +/- 197 pg/mL, P = .04). Urine phosphate excretion was significantly higher on day 7 in DM patients only (P < .05). Conclusions: PTH seems to play the major role in the regulation of phosphate excretion in DM CKD. The role of FGF-23 in phosphate disposal in DM CKD remains debatable.