POST-TRANSPLANT PHOSPHATURIA: DURATION AND PATHOGENESIS

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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).