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Nat. Rev. Nephrol. doi:10.1038/nrneph.2015.153 Figure 3 Development of hypophosphataemia and hyperphosphataemia after kidney transplantation Figure 3 | Development of hypophosphataemia and hyperphosphataemia after kidney transplantation. a | Under normal conditions, phosphate is freely filtered by the glomerulus; ∼70% of all filtered phosphate is reabsorbed by proximal tubular epithelial cells. Shortly after successful kidney transplantation, the filtered phosphate load is high. As a consequence of high FGF-23 and PTH levels, the abundance of NaPi-IIa and NaPi-IIc transporters in the luminal membrane of proximal tubular epithelial cells is suppressed, resulting in low phosphate reabsorption. Immunosuppressive medication, ischaemia–reperfusion injury, and metabolic acidosis also reduce phosphate reabsorption. Together, these factors stimulate phosphaturia, resulting in post-transplantation hypophosphataemia. b | With impaired graft function, a reduced glomerular filtered phosphate load results in less phosphate being offered to the proximal tubule. Phosphate reabsorption is reduced by high circulating levels of FGF-23 and PTH, in an attempt to stimulate phosphaturia. Immunosuppressive medication and metabolic acidosis might also reduce phosphate reabsorption. These factors are, however, unable to induce adequate phosphaturia and, therefore, result in progressive hyperphosphataemia, hyperparathyroidism, and excessively high FGF-23 levels. Similar mechanisms contribute to the development of hyperphosphataemia in the pre-transplantation chronic kidney disease setting. Abbreviations: GFR, glomerular filtration rate; I/R, ischaemia–reperfusion; mTOR, mammalian target of rapamycin; PTH, parathyroid hormone; Tx, transplantation. Baia, L. C. et al. (2015) Phosphate and FGF-23 homeostasis after kidney transplantation Nat. Rev. Nephrol. doi:10.1038/nrneph.2015.153