A new Hyperphosphatemia Drug

Abstract

Chronic renal failure has an average prevalence of 10% in the general population and carries a significant burden of morbidity and mortality. Moreover, the recently appreciated cross-talk between bone and the kidney is considered to be involved, when deranged, in the process of ectopic and vascular calcification. By disrupting this cross-talk, renal insufficiency can be responsible for cardiovascular disease. Vascular calcifications, which are increased in renal insufficiency, are also considered a major cause of cardiovascular disease. Hyperphosphatemia or an excessive phosphate burden in general is regarded as a formidable pathogenetic factor. We have known since many years that, by regulating tubular filtration and excretion, renal function plays a principal role in phosphate homeostasis. Also, in more recent years we have learned that the kidney synthesizes Klotho, a coreceptor of FGF23 which, in turn, is a major phosphate-regulating hormone produced by osteocytes. With these premises, hyperphosphatemia has taken center stage in renal patients and the attention to treatment of hyperphosphatemia has increased. In fact, the number of available oral phosphate binders has grown and a new class of iron-based drugs is emerging. Given the metal nature of iron and its positive charge, it is not surprising that iron is a powerful phosphate binder. Two such drugs have been approved for use in renal patients: sucroferric oxyhydroxide (or PA21) and iron citrate. Since only the former is available in Italy, we limited the present review to the analysis of the available clinical data useful to recognize the strengths and limitations of this new drug.