The control of hyperphosphatemia in chronic kidney disease: Which phosphate binder?

被引:3
作者
Ketteler, Markus [1 ]
机构
[1] Klinikum Coburg, Nephrol Klin, Div Nephrol, Coburg Clin, D-96450 Coburg, Germany
关键词
Calcium; Phosphate; PTH; Calcification; FGF23; Phosphatonins; CORONARY-ARTERY CALCIFICATION; HEMODIALYSIS-PATIENTS; MINERAL METABOLISM; CALCIUM-CARBONATE; SERUM PHOSPHORUS; MORTALITY RISK; RENAL-FAILURE; SEVELAMER; LANTHANUM; PROGRESSION;
D O I
10.1177/039139880903200206
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Hyperphosphatemia is currently regarded as a key mortality risk predictor in late CKD stages and especially in patients on dialysis. Fortunately, the armatorium to effectively treat hyperphosphatemia in end-stage renal disease has grown in recent years, and we gained an improved understanding of potential benefits and harms of specific compounds. Most interestingly, novel insights into the pathophysiology of calcium and phosphate handling, especially, the discovery of the phosphatonin FGF23, suggest a more complex assessment of phosphate balance especially in predialysis stages is warranted. This assessment should probably include measurements of fractional phosphate excretion and phosphatonin levels to objectively judge and effectively correct phosphate overload, however, clinical data on calcium and phosphate metabolism in CKD stages 3 - 4 are still scarce. This overview will both discuss aspects of pathophysiology of phosphate regulation and current and future clinical treatement approaches. (Int J Artif Organs 2009; 32: 95-100)
引用
收藏
页码:95 / 100
页数:6
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