2014年12月28日星期日

Hazards in the treatment of chronic kidney disease hyperphosphatemia

CKD treatment 
Hazards in the treatment of chronic kidney disease hyperphosphatemia

CKD treatment induced calcium and phosphorus metabolism and bone disease increased the risk of death

Calcium and phosphorus metabolism in early CKD had started. It has been observed before serum creatinine increased, that elevated serum phosphorus, calcium reduced, or even be seen in the histological changes of bone disease.

Closely related to serum phosphorus and CKD progression of the disease. Hyperphosphatemia can accelerate existing renal dysfunction.

Hyperphosphatemia is an independent risk factor for increased mortality in patients with end-stage renal disease. Hyperphosphatemia in hemodialysis patients can make long-term risk of death increased by 27 percent; hyperphosphatemia can increase the risk of death by 41% long-term hemodialysis patients with coronary artery disease. Elevated serum phosphorus per 1mmol / L, the risk of death than will rise 56%. Today, as the international community has hyperphosphatemia in dialysis patients with advanced CKD important predictor of mortality

Related CKD hyperphosphatemia treatment strategies

Clear limit phosphorus intake and dialysis efficacy exists limited or poor titer insufficient, the new non-calcium, non-aluminum phosphate binders (sevelamer), although showing good future prospects, but has yet to be greater scale clinical validation.

Today phosphate binders in the fight against hyperphosphatemia still occupy an important position. Since the beginning of the 1970s, the use of phosphate binders have become end-stage renal disease (ESRD) patients with hyperphosphatemia control standard therapy, which allows the intestinal absorption of phosphorus to 30% to 40%. Which contains calcium and phosphorus binders as the main force, is one of the key drugs in patients with chronic kidney disease hyperphosphatemia, hypocalcemia except to correct itself, mainly by limiting phosphorus absorption and prevent hyperphosphatemia occurs.

Currently containing calcium and phosphorus binders major clinical use of calcium carbonate and calcium acetate, both control serum phosphorus quite effective; but with low calcium dialysate calcium carbonate (1.25 mmol / L) can be a good control of serum phosphate concentration, to avoid taking calcium acetate dialysis patients the risk of muscle cramps occur easily, while calcium carbonate, calcium acetate, compared with a price advantage, often preferred clinic. Calcium carbonate is effective enough to reduce serum phosphorus guarantee.

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