When renal function diminishes, secondary hyperparathyroidism with develop in response
to worsening of kidney function and declined phosphate excretion (1). Dysregulation of
phosphorous and calcium homeostasis leads to decreased kidney phosphate excretion,
raised serum phosphorous, reduced synthesis of calcitriol, and elevated levels of the
phosphatonin fibroblast growth factor 23 (FGF-23)(2-4). These alterations result in
parathyroid hyperplasia and enhanced synthesis and secretion of parathyroid hormone
