Salivary Phosphorus Binding

Abstract

Hyperphosphatemia as a complication of chronic kidney disease (CKD) was recognized nearly a century ago.1 The central role of altered phosphate metabolism in CKD as a cause of secondary hyperparathyroidism and renal osteodystrophy was exposed as part of the elegant experimental studies that provided the basis of the “intact nephron hypothesis.”2 The association of high serum phosphorus levels and increased mortality of patients with ESRD first noted in 19903 has since been confirmed and extensively studied.4,5 There is now considerable evidence, convincing on balance, that elevated serum phosphorus levels are a surrogate marker of cardiovascular disease (coronary, aortic, valvular, and vascular calcification) and hard clinical outcomes (cardiovascular and all-cause hospitalization and mortality) in CKD.4–6 Accrued evidence on the systemic complications of altered phosphate homeostasis in CKD has led to the proposal of a new syndrome of mineral and bone disorders (MBD) of CKD, termed CKD-MBD, which encompasses biochemical alterations, bone abnormalities, and vascular calcification.7 Renewed interest in the detrimental consequences of elevated serum phosphorus and the difficulties of its management in CKD has become the center of much recent debate and controversy fueled, at least in part, by the pharmaceutical industry. Approximately two thirds of the daily phosphorus intake is absorbed in the small intestines, and normal phosphorus homeostasis is maintained by its subsequent appropriate excretion by the kidney.8 With decreasing kidney function, the initial adaptive changes for maintenance of …