Fibroblast growth factor 23 and calcium phosphate homeostasis after pediatric renal transplantation.

FGF23 is a circulating factor regulating TPR and is increased in CKD. After RT, it seems to induce phosphorus wasting in adults. Data on FGF23 after PRT are scarce. Parameters of bone metabolism including calcium, phosphate, 25-(OH) vitamin D, 1,25-(OH)(2) vitamin D, alkaline phosphatase, PTH, and FGF23 were analyzed in 57 children after PRT and 11 controls. Median time after PRT was 25.9 (range 2-135) months. eGFR after PRT ranged from 15 to 175 mL/min/1.73 qm. Mean (±s.e.) FGF23 and PTH levels were significantly elevated compared with controls (146 ± 30 vs. 43 ± 3 ng/L, p = 0.001 and 182 ± 42 vs. 74 ± 18 ng/L, p = 0.004, respectively). Highest FGF23 levels were found in children with an eGFR below 60 mL/min*1.73 sqm (280 ± 69 vs. 62 ± 5 ng/L, p = 0.001), but significantly elevated values were already present in CKD2T. In a multivariate analysis, eGFR, PTH, calcium, and phosphate were significantly associated with FGF23. In a subgroup of 17 patients (29.8%) with persistent hypophosphatemia, phosphate levels were significantly associated with FGF23 and not with PTH. FGF23 is increased in children after PRT, especially in patients with chronic allograft dysfunction, and seems to be a more sensitive marker of dysregulated calcium phosphate homeostasis than PTH.