Disturbances of mineral metabolism are among the most challenging clinical problems for patients with end-stage renal disease (ESRD). Beginning in its early stages, chronic kidney disease increases circulating concentrations of fibroblast growth factor 23 (FGF23), which triggers calcitriol (ie, 1,25-dihydroxyvitamin D3) deficiency, lowers serum calcium concentrations, and secondarily increases parathyroid hormone (PTH) levels.1 Simultaneously, progressive declines in glomerular filtration rate reduce phosphate excretory capacity, which further exacerbates FGF23 excess and secondary hyperparathyroidism. As advanced chronic kidney disease progresses to ESRD, hyperphosphatemia ensues, and FGF23 and PTH levels increase exponentially as they futilely work to overcome the impediments to normal mineral homeostasis imposed by loss of kidney function.
Middleton JP, Wolf M. Second Chances to Improve ESRD Outcomes With a Second-Generation Calcimimetic. JAMA. 2017;317(2):139-141. doi:10.1001/jama.2016.18631