Post-transplant hypophosphatemia:: Tertiary 'hyper-phosphatoninism'?
Post-transplant hypophosphatemia:: Tertiary 'hyper-phosphatoninism'?
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DOI：
10.1038/sj.ki.5001788
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发表时间：
2006-10-01
影响因子：
19.6
通讯作者：
Wolf, M.
中科院分区：
文献类型：
--
作者：
Bhan, I.;Shah, A.;Wolf, M.
低磷血症是肾移植术后常见的并发症。三级甲状旁腺功能亢进长期以来被认为是病因，但低磷酸盐血症可发生，尽管甲状旁腺激素（PTH）水平低，并可持续高PTH水平正常化后。此外，即使在移植物功能正常、低磷酸盐血症和甲状旁腺功能亢进的情况下，骨化三醇水平在移植后仍然不适当地低，表明PTH以外的机制起作用。成纤维细胞生长因子-23（FGF-23）诱导磷酸尿，抑制骨化三醇合成，并在慢性肾脏疾病中蓄积。我们对27例活体供肾移植受者进行了一项前瞻性纵向研究，以检验肾移植后过量FGF-23导致低磷血症和骨化三醇水平降低的假设。85%的受试者出现低磷血症< 2.5mg/dl，包括一名既往接受过甲状旁腺切除术的受试者; 37%出现磷酸盐血症
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 < 2.5mg/dl developed in 85% of subjects, including one who had previously undergone parathyroidectomy; 37% developed phosphate