Calcium in Chronic Kidney Disease

Abstract

The kidneys, through proximal tubular active uptake or pass-through of filtered phosphorus, regulate phosphorus homeostasis in healthy individuals. Hormones and factors that contribute to the kidney regulation of phosphorus include parathyroid hormone, 1,25-dihydroxyvitamin D (1,25(OH)2D), and fibroblast growth factor-23 (FGF-23). However, in patients with progressive chronic kidney disease (CKD), the normal homeostatic mechanisms are challenged as FGF-23 and parathyroid hormone rise and 1,25(OH)2D levels decline. Certainly, by late stage 4 CKD and into ESRD, most of these patients exhibit frank hyperphosphatemia and have secondary hyperparathyroidism, marked elevations of FGF-23, and 1,25(OH)2D deficiency. These changes in normal phosphate homeostasis lead in part to the manifestations of the entity known as CKD–mineral bone disorder (CKD-MBD) (1). Epidemiologic data have identified an association between the hyperphosphatemia of CKD-MBD and patient-based outcomes of vascular calcification, myocardial dysfunction, and mortality (2–5). The management of hyperphosphatemia is currently based on a combination of three measures: dietary phosphorus restriction, dialysis, and the use of phosphate binders. The importance of phosphorus in the poor patient outcomes associated with untreated CKD-MBD is supported by the evidence that reduction of serum phosphorus, through the use of dietary phosphorus binders, improves patient survival (6–8). Our supplement, which is based on a conference held in Montreal in September 2008, focuses on some of the prevailing controversies regarding dietary phosphorus binders, leading to our symposium theme: “Myths and Realities of Calcium in CKD.” Historically, hyperphosphatemia was first treated with aluminum-based dietary phosphate binders, for which aluminum hydroxide was widely …