FGF23 Beyond Mineral Metabolism: A Bridge to Cardiovascular Disease

摘要

One of the largest challenges in current clinical nephrology is to alleviate the massive increment in cardiovascular comorbidity in the chronic kidney disease (CKD) population. Over the past decade, a particular focus has been directed at optimizing treatment of disordered mineral metabolism, which, in innumerous scientific reports, is linked to cardiovascular disease and reduced survival. Defining the true culprits is, however, a complex matter, since all components of mineral metabolism (i.e., inorganic phosphate [Pi]), calcium, parathyroid hormone [PTH], and vitamin D) influence each other through intricate physiologic feedback loops. In other words, intervention against one of these factors will inevitably invoke alterations in all of the others. That, in combination with a lack of randomized placebo-controlled trials, has sparked a never-ending debate on the optimal strategies for intervention against disordered mineral metabolism, forcing clinicians to rely upon the use of nonvalidated surrogate markers and treatment guidelines based on observational data.