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Post-transplant hypophosphatemia: Tertiary 'Hyper-Phosphatoninism'?
Kidney Int. 2006 Oct; 70(8):1486-94.KI

Abstract

Hypophosphatemia is a common complication of kidney transplantation. Tertiary hyperparathyroidism has long been thought to be the etiology, but hypophosphatemia can occur despite low parathyroid hormone (PTH) levels and can persist after high PTH levels normalize. Furthermore, even in the setting of normal allograft function, hypophosphatemia, and hyperparathyroidism, calcitriol levels remain inappropriately low following transplantation, suggesting that mechanisms other than PTH contribute. Fibroblast growth factor-23 (FGF-23) induces phosphaturia, inhibits calcitriol synthesis, and accumulates in chronic kidney disease. We performed a prospective, longitudinal study of 27 living donor transplant recipients to test the hypotheses that excessive FGF-23 accounts for hypophosphatemia and decreased calcitriol levels following kidney transplantation. Hypophosphatemia <2.5 mg/dl developed in 85% of subjects, including one who had previously undergone parathyroidectomy; 37% developed phosphate < or =1.5 mg/dl. The mean pre-transplant FGF-23 level was 1,218+/-542 RU/ml. Within the first week following transplantation, mean levels decreased to 557+/-579 RU/ml, which were still above normal. FGF-23 was independently associated with serum phosphate (P < 0.01), urinary excretion of phosphate (P < 0.01), and calcitriol levels (P < 0.01); PTH was not independently associated with any of these parameters. We calculated area under the curve for FGF-23 and PTH between the pre- and first post-transplant levels as a summary measure of early exposure to these phosphaturic hormones. An area under the FGF-23 curve greater than the median was associated with a relative risk of developing hypophosphatemia < or =1.5 mg/dl of 5.3 (P = 0.02) compared with lower levels. Increased area under the PTH curve was not associated with greater risk of hypophosphatemia. Excessive FGF-23 exposure in the early post-transplant period appears to be more strongly associated with post-transplant hypophosphatemia than PTH.

Authors+Show Affiliations

Renal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16941023

Citation

Bhan, I, et al. "Post-transplant Hypophosphatemia: Tertiary 'Hyper-Phosphatoninism'?" Kidney International, vol. 70, no. 8, 2006, pp. 1486-94.
Bhan I, Shah A, Holmes J, et al. Post-transplant hypophosphatemia: Tertiary 'Hyper-Phosphatoninism'? Kidney Int. 2006;70(8):1486-94.
Bhan, I., Shah, A., Holmes, J., Isakova, T., Gutierrez, O., Burnett, S. M., Jüppner, H., & Wolf, M. (2006). Post-transplant hypophosphatemia: Tertiary 'Hyper-Phosphatoninism'? Kidney International, 70(8), 1486-94.
Bhan I, et al. Post-transplant Hypophosphatemia: Tertiary 'Hyper-Phosphatoninism'. Kidney Int. 2006;70(8):1486-94. PubMed PMID: 16941023.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Post-transplant hypophosphatemia: Tertiary 'Hyper-Phosphatoninism'? AU - Bhan,I, AU - Shah,A, AU - Holmes,J, AU - Isakova,T, AU - Gutierrez,O, AU - Burnett,S M, AU - Jüppner,H, AU - Wolf,M, Y1 - 2006/08/30/ PY - 2006/8/31/pubmed PY - 2006/11/9/medline PY - 2006/8/31/entrez SP - 1486 EP - 94 JF - Kidney international JO - Kidney Int VL - 70 IS - 8 N2 - Hypophosphatemia is a common complication of kidney transplantation. Tertiary hyperparathyroidism has long been thought to be the etiology, but hypophosphatemia can occur despite low parathyroid hormone (PTH) levels and can persist after high PTH levels normalize. Furthermore, even in the setting of normal allograft function, hypophosphatemia, and hyperparathyroidism, calcitriol levels remain inappropriately low following transplantation, suggesting that mechanisms other than PTH contribute. Fibroblast growth factor-23 (FGF-23) induces phosphaturia, inhibits calcitriol synthesis, and accumulates in chronic kidney disease. We performed a prospective, longitudinal study of 27 living donor transplant recipients to test the hypotheses that excessive FGF-23 accounts for hypophosphatemia and decreased calcitriol levels following kidney transplantation. Hypophosphatemia <2.5 mg/dl developed in 85% of subjects, including one who had previously undergone parathyroidectomy; 37% developed phosphate < or =1.5 mg/dl. The mean pre-transplant FGF-23 level was 1,218+/-542 RU/ml. Within the first week following transplantation, mean levels decreased to 557+/-579 RU/ml, which were still above normal. FGF-23 was independently associated with serum phosphate (P < 0.01), urinary excretion of phosphate (P < 0.01), and calcitriol levels (P < 0.01); PTH was not independently associated with any of these parameters. We calculated area under the curve for FGF-23 and PTH between the pre- and first post-transplant levels as a summary measure of early exposure to these phosphaturic hormones. An area under the FGF-23 curve greater than the median was associated with a relative risk of developing hypophosphatemia < or =1.5 mg/dl of 5.3 (P = 0.02) compared with lower levels. Increased area under the PTH curve was not associated with greater risk of hypophosphatemia. Excessive FGF-23 exposure in the early post-transplant period appears to be more strongly associated with post-transplant hypophosphatemia than PTH. SN - 0085-2538 UR - https://www.unboundmedicine.com/medline/citation/16941023/Post_transplant_hypophosphatemia:_Tertiary_'Hyper_Phosphatoninism' L2 - https://linkinghub.elsevier.com/retrieve/pii/S0085-2538(15)52165-0 DB - PRIME DP - Unbound Medicine ER -