INTRODUCTIONPhosphate homoeostasis is maintained by a counterbalance between dietary phosphate absorption by the intestine, mobilization from bone, and renal excretion: the so‐called bone–kidney endocrine axis. Endocrine factors, including the classical mineral metabolism components, vitamin D and parathyroid hormone (PTH), and also the newer nonclassical mineral metabolism components, fibroblast growth factor (FGF)‐23 and its co‐receptor klotho, are intimately involved in the control of systemic phosphate homoeostasis. Alterations in these components have been traditionally circumscribed to patients with renal disease; however, in the last decades, a large number of clinical and basic/experimental studies have provided evidence that abnormalities in these mineral components can also trigger important and even independent cardiotoxic effects. Accordingly, it is now known that changes to the levels of these systemic mineral components increase, directly and indirectly, cardiovascular (CV) risk in patients with chronic kidney disease (CKD). Beyond the nephropathological context, these changes are also independently associated with clinical cardiac disease and its complications, including left ventricular hypertrophy (LVH), heart failure (HF) and atrial fibrillation (AF), among others. For instance, a deficiency in vitamin D is considered a predictor of reduced survival in patients with HF. Similarly, several recent prospective trials and meta‐analyses have shown that supraphysiological circulating
European Journal of Clinical Investigation – Wiley
Published: Jan 1, 2018
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