[Clinical aspect of recent progress in phosphate metabolism. Pathophysiology of secondary hyperparathyroidism in chronic kidney disease].

Secondary hyperparathyroidism is one of the most popular complications in patients with chronic kidney disease. Phosphate retention, decreasing 1,25-dihydroxyvitamin D3, and hypocalcemia with kidney dysfunction stimulate the secretion of parathyroid hormone. Persistent hyperparathyroidism leads to the development of parathyroid hyperplasia, thereby resisting to medical therapy. Fibroblast growth factor (FGF) 23, which is the novel phosphaturic hormone, increases in patients with chronic kidney disease. In the early stage of chronic kidney disease, high serum FGF23 levels increase the excretion of phosphate, thereby improving hyperphosphatemia due to chronic kidney disease. However, it is not fully elucidated how high serum FGF23 levels effect secondary hyperparathyroidism in end-stage renal failure. Further studies will be necessary to clarify the pathophysiology of secondary hyperparathyroidism in chronic kidney disease.