Calcium in Chronic Kidney Disease: Myths and Realities

[摘要] 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).

[学科分类] 泌尿医学

[关键词] Bone marrow necrosis;Sickle cell disease;Hyperhemolysis syndrome