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Tertiary ‘Hyperphosphatoninism’ Accentuates Hypophosphatemia and Suppresses Calcitriol Levels in Renal Transplant Recipients
Author(s) -
Evenepoel P.,
Naesens M.,
Claes K.,
Kuypers D.,
Vanrenterghem Y.
Publication year - 2007
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2007.01753.x
Subject(s) - hypophosphatemia , calcitriol , fibroblast growth factor 23 , medicine , endocrinology , transplantation , parathyroid hormone , creatinine , vitamin d and neurology , calcium
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 (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.