Hypophosphatemia and inappropriately low
calcitriol levels are frequently observed following successful
renal transplantation.
Fibroblast growth factor-23 (FGF-23) is a recently characterized phosphaturic
hormone that inhibits renal 1 alpha-
hydroxylase activity and may be involved in the pathogenesis of both phenomena. The following hypotheses were tested: pretransplant FGF-23 predicts posttransplant FGF-23, FGF-23 predicts posttransplant
hypophosphatemia and FGF-23 is associated with decreased
calcitriol levels independent of renal and parathyroid function. Serum biointact
parathyroid hormone (PTH),
calcidiol,
calcitriol, full-length FGF-23,
calcium and
phosphate were monitored in 41 renal transplant recipients at the time of
transplantation (pre) and 3 months thereafter (post). In addition, serum
phosphate nadir in each individual patient was identified and urinary fractional excretion of
phosphate (FE(PO4)) at month 3 was calculated. High FGF-23(post) levels were independently associated with high FGF-23(pre), low
calcitriol(post) and high
calcium(post) levels. FGF-23, but none of the other
mineral metabolism indices, was an independent predictor of the
phosphate nadir in the early posttransplant period. A high FGF-23(post) level was independently associated with a high FE(PO4). High FGF-23(post) and
creatinine levels and low PTH(post) levels were independently associated with low
calcitriol(post) levels. In conclusion, our data indicate that persistence of FGF-23 contributes to
hypophosphatemia and suboptimal
calcitriol levels in renal transplant recipients.