Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)

Abstract

In the early stages of chronic kidney disease, serum phosphorus levels are maintained within the normal range by a compensatory increase in parathyroid hormone and fibroblast growth factor 23, which inhibits reabsorption of phosphorus by the proximal renal tubules. However, as chronic kidney disease progresses, the risk of overt hyperphosphatemia also increases as the limit of the kidney's ability to excrete phosphorus is reached. In addition to abnormalities in the serum phosphorus profile, abnormalities of chronic kidney disease-mineral and bone disorder include those of bone turnover, mineralization, volume, and growth and of vascular calcification. Indeed, the co-localization of osteoblast-like cells and bone markers, such as osteopontin, alkaline phosphatase, and osteocalcin, in the arterial walls of patients with uremia indicates that vascular calcification is an active biological process with analogies to bone mineralization. To prevent hyperphosphatemia, patients with end-stage renal disease limit their intake of foods that are naturally high in phosphorus. However, phosphorus-containing additives are increasingly found in processed foods and fast foods. Therefore, educating patients with end-stage renal disease to avoid phosphorus-containing food additives results in modest improvements in hyperphosphatemia. We tend not to routinely measure serum phosphorus levels in patients. However, we should measure serum phosphorus levels to clarify the effect of serum phosphorus on vascular calcification and mortality, even in patients without chronic kidney disease.