Dialyse aktuell 2011; 15(08): 468-470
DOI: 10.1055/s-0031-1291970
Forum der Industrie
Georg Thieme Verlag KG Stuttgart · New York

Phosphatstörungen bei chronisch nierenkranken Patienten – Wann müssen Interventionen beginnen?

Further Information

Publication History

Publication Date:
04 October 2011 (online)

Also available at
 

Die gestörte Phosphatbalance bei Patienten mit chronischer Nierenerkrankung (CKD: "chronic kidney disease") war ein zentrales Thema auf dem 48. Kongress der ERA-EDTA ("European Renal Association – European Dialysis and Transplant Association") in Prag Ende Juni. Ein Symposium des Biotechnologieunternehmens Genzyme, das unter dem Titel "Phosphate Dysregulation in Chronic Kidney Disease in 2011: What’s next?" stand, gab ein umfassendes Update zur Früherkennung und Therapie der Hyperphosphatämie.

2 Renagel in New Dialysis Patients


 

  • Literatur

  • 1 Larson T, Nisbeth U, Ljunggren O et al. Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. Kidney Int 2003; 64: 2273-2279
    Google Scholar
  • 2 Gutiérrez O, Isakova T, Rhee E et al. Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. J Am Soc Nephrol 2005; 16: 2205-2215
    CrossrefGoogle Scholar
  • 3 Gutiérrez OM, Januzzi JL, Isakova T et al. Fibroblast growth factor 23 and left ventricular hypertrophy in chronic kidney disease. Circulation 2009; 119: 2545-2552
    CrossrefGoogle Scholar
  • 4 Gutiérrez OM, Mannstatt M, Isakova T et al. Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis. N Engl J Med 2008; 359: 584-592
    CrossrefGoogle Scholar
  • 5 Wolf M, Molnar MZ, Amaral AP et al. Elevated fibroblast growth factor 23 is a risk factor for kidney transplant loss and mortality. J Am Soc Nephrol 2011; 22: 956-966
    CrossrefGoogle Scholar
  • 6 Nagano N, Miyata S, Abe M et al. Effect of manipulating serum phosphorus with phosphate binder on circulating PTH and FGF23 in renal failure rats. Kidney Int 2006; 69: 531-537
    CrossrefGoogle Scholar
  • 7 Koiwa F, Kazama JJ, Tokumoto A et al. Sevelamer hydrochloride and calcium bicarbonate reduce serum fibroblast growth factor 23 levels in dialysis patients. Ther Apher Dial 2005; 9: 336-339
    CrossrefGoogle Scholar
  • 8 Oliveira RB, Cancela AL, Graciolli FG et al. Early control of PTH and FGF23 in normophosphatemic CKD patients: a new target in CKD-MBD therapy?. J Am Soc Nephrol 2010; 5: 286-291
    CrossrefGoogle Scholar
  • 9 Isakova T, Wahl P, Vargas SG et al. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease. Kidney Int 2011; 79: 1370-1378
    CrossrefGoogle Scholar
  • 10 Kestenbaum B, Sampson JN, Rudser KD et al. Serum phosphate levels and mortality risk among people with chronic kidney disease. J Am Soc Nerphrol 2005; 16: 520-528
    Google Scholar
  • 11 Shroff RC, McNair R, Skepper JN et al. Chronic mineral dysregulation promotes vascular smooth muscle cell adaptation and extracellular matrix calcification. J Am Soc Nephrol 2010; 21: 103-112
    CrossrefGoogle Scholar
  • 12 Block GA, Spiegel DM, Ehrlich J et al. Effects of sevelamer and calcium on coronary artery calcification in patients new to hemodialysis. Kidney Int 2005; 68: 1815-1824
    CrossrefGoogle Scholar
  • 13 Ketteler M, Biggar PH. As nature did not predict dialysis--what we can learn from FGF23 in end-stage renal disease?. Nephrol Dial Transplant 2009; 24: 2618-2620
    CrossrefGoogle Scholar
  • 14 Isakova T, Gutiérrez OM, Chang Y et al. Phosphorus binders and survival on hemodialysis. J Am Soc Nephrol 2009; 20: 388-396
    CrossrefGoogle Scholar
  • 15 Russo D, Miranda I, Ruocco C et al. The progression of coronary artery calcification in predialysis patients on calcium carbonate or sevelamer. Kidney Int 2007; 72: 1255-1261
    CrossrefGoogle Scholar
  • 16 Ketteler M, Rix M, Fan S et al. Efficacy and tolerability of sevelamer carbonate in hyperphosphatemic patients who have chronic kidney disease and are not on dialysis. Clin J Am Soc Nephrol 2008; 3: 1125-1130
    CrossrefGoogle Scholar
  • 17 Bushinsky DA. Contribution of intestine, bone, kidney, and dialysis to extracellular fluid calcium content. Clin J Am Soc Nephrol 2010; 5 (Suppl. 01) 12-22
    CrossrefGoogle Scholar
  • 18 Pun HP, Lehrich RW, Honeycutt EF et al. Modifiable risk factors associated with sudden cardiac arrest within hemodialysis clinics. Kidney Int 2011; 79: 218-227
    CrossrefGoogle Scholar