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Eur J Endocrinol. 2011 May;164(5):839-47. doi: 10.1530/EJE-10-1150. Epub 2011 Feb 18.

Early post-transplantation hypophosphatemia is associated with elevated FGF-23 levels.

Author information

1
Department of Internal Medicine Service of Transplantation, University Hospitals, Geneva 14, Switzerland. andrea.trombetti@unige.ch

Abstract

BACKGROUND:

We examined the hypothesis that high FGF-23 levels early after transplantation contribute to the onset of hypophosphatemia, independently of parathyroid hormone (PTH) and other factors regulating phosphate metabolism.

METHODS:

We measured serum phosphate levels (sPi), renal tubular reabsorption of Pi (TmPi/GFR), estimated GFR (eGFR), intact PTH (iPTH), calcitriol, intact (int) and C-terminal (Cter) FGF-23, dietary Pi intake and cumulative doses of glucocorticoids in 69 patients 12 days (95% confidence interval, 10-13) after renal transplantation.

RESULTS:

Hypophosphatemia was observed in 43 (62%) of the patients 12 days after transplantation. Compared with non-hypophosphatemic subjects, their post-transplantation levels of intact and CterFGF-23 were higher (195 (108-288) vs 48 (40-64) ng/l, P<0.002 for intFGF-23; 205 (116-384) vs 81 (55-124) U/ml, P<0.002, for CterFGF-23). In all subjects, Cter and intFGF-23 correlated inversely with sPi (r=-0.35, P<0.003; -0.35, P<0.003, respectively), and TmPi/GFR (r=-0.50, P<0.001; -0.54, P<0.001, respectively). In multivariate models, sPi and TmPi/GFR were independently associated with FGF-23, iPTH and eGFR. Pre-transplant iPTH levels were significantly higher in patients developing hypophosphatemia after renal transplantation. Pre-transplant levels of FGF-23 were not associated with sPi at the time of transplantation.

CONCLUSION:

In addition to PTH, elevated FGF-23 may contribute to hypophosphatemia during the early post-renal transplant period.

PMID:
21335460
DOI:
10.1530/EJE-10-1150
[Indexed for MEDLINE]
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