POST-TRANSPLANT PHOSPHATURIA: DURATION AND PATHOGENESIS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 假设：尽管肾移植术后血磷恢复正常，但肾移植患者仍持续存在肾磷损耗和磷负平衡。成纤维细胞生长因子-23(FGF-23)和前列腺素E-2(PGE-2)在肾移植后低磷血症肾小管磷重吸收中起致病作用，抑制PGE2的合成可以部分纠正这一缺陷。 为了验证上述假设，调查人员将通过四种方法实现以下目标： 目的1：在血磷正常的肾移植受者移植后12个月至24个月的代谢研究中，确定实际的磷平衡。 目的2：在横断面研究中评估肾移植后受试者TMPo4/GFR、成纤维细胞生长因子-23和前列腺素E_2的相关性。 目的：在前瞻性纵向研究中确定移植后受者TMPo4/GFR和尿PGE2的自然史。 目的：通过测定口服或口服omega-3多不饱和脂肪酸乙酯[二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)](鱼油)抑制前列腺素E_2(PGE_2)合成前后血浆成纤维细胞生长因子-23(FGF-23)、尿前列腺素E_2(PGE_2)水平和TMPo4/GFR，对移植后受者进行干预研究。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Hypothesis: Renal transplant patients continue to have renal phosphorus wasting and negative phosphorus balance despite the normalization of serum phosphorus after renal transplantation. Fibroblast Growth Factor-23 (FGF-23) and or prostaglandin E-2 (PGE-2play a pathogenetic role in defective renal tubular phosphorus reabsorption in post-renal transplant hypophosphatemia and inhibition of synthesis of PGE2 can partially correct this defect. To test the above hypothesis, the investigators will achieve the following objectives with four approaches: Aim 1: To determine actual phosphorous balance in a metabolic study in post-renal transplantation subjects, 12 months to 24 months post-transplantation, with normal serum phosphorous. Aim 2: To evaluation post-renal transplantation subjects in a cross sectional study for a correlation between TMPo4/GFR, FGF-23, and PGE2. Aim 3: To determine in a prospective longitudinal study the natural history of TMPo4/GFR, and urinary PGE2 in post-transplantation subjects. Aim 4: To conduct an interventional study in post-transplantation subjects by measuring plasma FGF-23 concentration, urinary PGE2 levels, and TMPo4/GFR before and after inhibition of PGE2 systhesis by administration or oral omega-3 polyunsaturated fatty acid ethyl esters [Eicosapentaonoic acid (EPA) and Docosahexaenoic acid (DHA)](Fish Oil).