鉄，アルミニウム，ランタン化合物と高リン血症治療

抄録

  The control of the serum phosphorus (P) level in chronic kidney disease patients is important because elevated serum P levels are associated with progression of vascular calcification and increased mortality in these patients. In 2014, a novel phosphate binder, ferric citrate hydrate (Riona^®), became available for the treatment of hyperphosphatemia in Japan, the first country to approve this medication. Ferric citrate hydrate, which relies upon the potent phosphate-binding capacity of ferric iron, inhibits P absorption by forming complexes between ferric iron and dietary phosphate in the gut. The active pharmaceutical ingredient in ferric citrate hydrate provides a larger specific surface area and higher water solubility; therefore, it is expected to have greater efficacy in terms of its phosphate-binding capacity. In clinical trials, ferric citrate hydrate significantly reduced the serum phosphate level and effectively maintained serum P concentrations throughout the duration of the trials. Moreover, in one clinical trial, ferric citrate hydrate significantly decreased levels of fibroblast growth factor-23 (FGF-23) in nondialysis patients. FGF-23 is an endocrine hormone that increases urinary phosphate excretion to maintain serum P at the proper level. A portion of the iron from ferric citrate hydrate is absorbed and transported throughout the body as transferrin-bound iron, where it is used for the synthesis of hemoglobin, enzymes, and others. Although safer and more effective phosphate binders are expected in the future, ferric citrate hydrate will become a new approach for the treatment of hyperphosphatemia.