Abstract:

ABSTRACT  Phosphorus is an important element in the life of the body in cellular metabolism and structure maintenance. Serum phosphorus is a direct reflection of phosphorus metabolism. The balance of phosphorus is decided by intestine absorption, kidney excretion, and body usage as well as a series of regulatory factors. In patients with chronic renal failure, this balance is broken. Patients often show high phosphorus status due to renal dysfunction and physical changes in endocrine function. Hyperphosphatemia has been proved to be related with renal osteodystrophy, vascular calcification, cardiovascular events incidence and mortality. Sodium phosphate co-transporter is the common channel to determine the phosphate transport in small intestine and renal tubular epithelial cells. It is divided into three subtypes. The impact factors of sodium phosphate co-transporter include diet, PTH, VitD3, FGF-23 and so on. The current means of control of hyperphosphatemia primarily are dialysis, diet restriction, and usage of phosphate binders. At the same time, the levels of serum calcium, PTH, and 1, 25(OH)2D3 are required to control. The latest K/DIGO guidelines recommend that in CKD3-4, serum calcium and phosphorus levels should be controlled within the normal range (calcium:8.5-10.5mg/dl, phosphorus 2.5-4.5mg/dl), while to CKD5 patients, serum phosphate should be as close to normal range. All treatment programs are determined according to the dynamic changes of patients' conditions, rather than a particular monitoring data.