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Tertiary ‘Hyperphosphatoninism’ Accentuates Hypophosphatemia and Suppresses Calcitriol Levels in Renal Transplant Recipients

P. Evenepoel,M. Naesens,K. Claes,D. Kuypers,Y. Vanrenterghem

Published 2007 in American Journal of Transplantation

ABSTRACT

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 1α‐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 (FEPO4) at month 3 was calculated. High FGF‐23post levels were independently associated with high FGF‐23pre, low calcitriolpost and high calciumpost 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‐23post level was independently associated with a high FEPO4. High FGF‐23post and creatinine levels and low PTHpost levels were independently associated with low calcitriolpost levels. In conclusion, our data indicate that persistence of FGF‐23 contributes to hypophosphatemia and suboptimal calcitriol levels in renal transplant recipients.

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