Phosphorus and Survival

Abstract

For more than forty years now, high serum phosphate levels, a highly prevalent condition in patients with chronic kidney disease (CKD), have been associated with the pathogenesis of secondary hyperparathyroidism, a common mineral and bone disorder (MBD).1 Recent epidemiologic and experimental studies have further amplified the role this condition plays in the larger story of CKD-MBD. Experimental studies have demonstrated that high phosphorus plays a key role in the development of vascular calcification2 and impairment of bone mass and strength, induces changes in the expression pattern of muscle and bone-related genes,3,4 and may also act as a pro-aging factor.5 In addition, clinical studies have demonstrated an association among hyperphosphatemia, vascular stiffness, and left ventricular hypertrophy.6 Taking all of the aforementioned findings together, it is reasonable to hypothesize all these untoward actions of phosphorus may ultimately affect mortality, as it has been suggested by several studies carried out in different dialysis cohorts.7,8 The increase in the importance of phosphorus in the spectrum of CKD-MBD also coincides with the description of the multiple actions of a new modulator, fibroblast growth factor 23 (FGF-23). This phosphatonin carries out some effects independent of phosphorus, such as its inhibitory effect on parathyroid hormone synthesis,9 but, so far, most of the biologic actions of FGF-23, including its recently described association with mortality,10 seem to be highly interdependent and related …