An unusual cause of elevated serum creatinine after kidney transplantation in an adolescent: Answers

Excerpt

Phosphate metabolism disorder is a very common problem in chronic kidney disease and is characterized by increased fibroblast growth factor (FGF)-23, secondary hyperparathyroidism and hyperphosphatemia. As the glomerular filtration rate (GFR) falls below < 60 ml/ min/1.73 m², FGF-23 expression in osteoblasts and osteocytes increases, and serum FGF-23 level rises in response to phosphate retention [1]. In the kidney, which is one of its main target organs, FGF-23 primarily acts on the proximal and distal convoluted renal tubules. It decreases active vitamin D production by inhibiting the expression of 1α-hydroxylase in the proximal tubules, and by this way, it inhibits phosphate reabsorption. In the distal convoluted tubules, FGF-23 increases reabsorption of calcium and sodium by increasing the apical membrane expression of the epithelial calcium channel and sodium-chloride cotransporter [2]. On the other hand, kidney transplantation creates a sudden change in the phosphate metabolism. Most transplant recipients develop hypophosphatemia in the first 3 months after transplantation due to unopposed high FGF-23 and PTH levels, secondary to their slow adaptation to a newly improved kidney function. Moreover, some immunosuppressive drugs may also have a phosphaturic effect [3]. Although the FGF-23 level was not assessed in our patient, she had significant hyperphosphatemia and secondary hyperparathyroidism in the pre-transplantation era. Since the PTH level was shown to be persistently high in the early period after kidney transplantation, hypophosphatemia developed in our patient. …