N utritional management has classically been regarded as an integral part of therapy for chronic kidney disease (CKD). 1,2,S1–S4 Various dietary constituents are consid- ered, 1,2 but, in the case of CKD? mineral and bone disorders (CKD-MBD), phosphorus (P) load and hyperphosphatemia have frequently been the focus of attention. Higher plasma P levels (even within the normal range) have been associated with increased risk of incident CKD, vascular calcifica- tion, and cardiovascular morbidity and mortality. 3 Moreover, the role of P load and/or hyperphosphatemia in the pathophysiology of secondary hyperparathyroidism, renal osteo- dystrophy, left ventricular hyper- trophy, accelerated progression of CKD, cardiovascular damage/ calcification, and aging—via both direct and indirect effects—is sup- ported by compelling epidemiologic and experimental evidence, and biologic plausibility.
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