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Tertiary 'hyperphosphatoninism' accentuates hypophosphatemia and suppresses calcitriol levels in renal transplant recipients.
Am J Transplant. 2007 May; 7(5):1193-200.AJ

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 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.

Authors+Show Affiliations

Department of Medicine, Division of Nephrology, University Hospital Leuven, B-3000 Leuven, Belgium. Pieter.Evenepoel@uz.kuleuven.ac.beNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article

Language

eng

PubMed ID

17359508

Citation

Evenepoel, P, et al. "Tertiary 'hyperphosphatoninism' Accentuates Hypophosphatemia and Suppresses Calcitriol Levels in Renal Transplant Recipients." American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons, vol. 7, no. 5, 2007, pp. 1193-200.
Evenepoel P, Naesens M, Claes K, et al. Tertiary 'hyperphosphatoninism' accentuates hypophosphatemia and suppresses calcitriol levels in renal transplant recipients. Am J Transplant. 2007;7(5):1193-200.
Evenepoel, P., Naesens, M., Claes, K., Kuypers, D., & Vanrenterghem, Y. (2007). Tertiary 'hyperphosphatoninism' accentuates hypophosphatemia and suppresses calcitriol levels in renal transplant recipients. American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 7(5), 1193-200.
Evenepoel P, et al. Tertiary 'hyperphosphatoninism' Accentuates Hypophosphatemia and Suppresses Calcitriol Levels in Renal Transplant Recipients. Am J Transplant. 2007;7(5):1193-200. PubMed PMID: 17359508.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tertiary 'hyperphosphatoninism' accentuates hypophosphatemia and suppresses calcitriol levels in renal transplant recipients. AU - Evenepoel,P, AU - Naesens,M, AU - Claes,K, AU - Kuypers,D, AU - Vanrenterghem,Y, Y1 - 2007/03/12/ PY - 2007/3/16/pubmed PY - 2007/8/8/medline PY - 2007/3/16/entrez SP - 1193 EP - 200 JF - American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons JO - Am J Transplant VL - 7 IS - 5 N2 - 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. SN - 1600-6135 UR - https://www.unboundmedicine.com/medline/citation/17359508/Tertiary_'hyperphosphatoninism'_accentuates_hypophosphatemia_and_suppresses_calcitriol_levels_in_renal_transplant_recipients_ L2 - https://doi.org/10.1111/j.1600-6143.2007.01753.x DB - PRIME DP - Unbound Medicine ER -