Control of serum phosphorus: implications for coronary artery calcification and calcific uremic arteriolopathy (calciphylaxis)

There is mounting evidence that elevated serum phosphorus is an important c ardiovascular risk factor in patients with end stage renal disease. Recent work has shown that vascular smooth muscle cells have the ability to underg o osteoblastic differentiation and produce an environment conducive to mine ralization. Serum phosphorus is an important stimulator of this process and the adverse cardiovascular effects of hyperphosphatemia are most likely me diated via its ability to enhance the development of vascular calcification . Arterial calcification, whether it is intimal or medial in location, is a strong independent risk factor for cardiovascular morbidity and mortality. Both coronary artery calcification and calciphylaxis are prototypical exam ples of arterial calcification that have been associated with poor phosphat e control. Furthermore, several investigators have recently suggested that the prescription of large doses of calcium to achieve phosphate control may augment, rather than diminish, the risk of vascular calcification. This is more likely to be true in the presence of low turnover bone disease, a dia gnosis difficult to make with routine laboratory testing. A brief review of the molecular biology of vascular calcification supports the concept that warfarin administration may exacerbate the calcific process, particularly i n the setting of hyperphosphatemia, as has been reported in patients with c alciphylaxis. Recognizing the consequences of poor phosphate control, it is time to adopt strict target levels that aim to normalize serum phosphorus levels. The available evidence supports that this control should not be ach ieved through the use of supraphysiologic doses of supplemental calcium. Cu rr Opin Nephrol Hypertens 10:741-747. (C) 2001 Lippincott Williams & Wilkin s.