Kovesdy CP, et al. Clin J Am Soc Nephrol. 2009;4:435–41. (Level 4) 2. Kalantar-Zadeh K, et al. J Am Soc Nephrol. 2005;16:3070–80. (Level 4) 3. Pollak VE, et al. BMC Nephrol. 2009;10:6. (Level 4) 4. Teehan GS, et al. Clin Infect Dis. 2004;38:1090–4. (Level 4) 5. Hasuike Y, et al. Clin Exp Nephrol. 2010;14:349–55. (Level 4) 6. Stancu S, et learn more al. Am J Kidney Dis. 2010;55:639–47. (Level 4) Are long-acting ESAs recommended for treatment of renal anemia in GKT137831 ic50 non-dialysis CKD? Recently, long-acting ESAs have become available. The advantage of these new ESAs was examined. Since long-acting ESAs have a longer half-life
as compared to recombinant human erythropoietin (rHuEPO), improving and maintaining the Hb level through a lower frequency of administration can be expected. At the same time, long-acting ESA might change the clinical outcome selleck inhibitor as a result of the different function and duration of activity. However, the latter is not clear at present. For the former statement, a cohort
study on darbepoetin alfa (DA) by Gobin et al. has been the only one to report that the frequency of administration necessary for achieving the target Hb was decreased by replacing rHuEPO with long-acting ESA in non-dialysis CKD. A randomized controlled trial comparing DA with rHuEPO has not been conducted, so the absolute superiority of DA over rHuEPO has not been demonstrated. The status of methoxy polyethylene glycol-epoetin beta is also the same. Although a randomized controlled trial has been conducted, it merely confirmed that administration every 4 weeks did not yield inferior results compared with administration every 2 weeks. As Niclosamide mentioned above, we conclude that currently there is no strong reason to recommend long-acting ESAs. Bibliography 1. Gobin J, et al. Clin Drug Investig. 2011;31:113–20. (Level 4) 2. Hertel J, et al. Am J Nephrol. 2006;355–26:149–56. (Level 4) 3. Disney A, et al. Nephrology. 2007;12:95–101.
(Level 4) 4. Agarwal AK, et al. J Intern Med. 2006;260:577–85. (Level 4) 5. Kessler M, et al. Hemodial Int. 2010;14:233–9. (Level 2) 6. Roger SD, et al. Nephrol Dial Transplant. 2011;26:3980–6. (Level 2) Chapter 8: CKD–Mineral and Bone Disorders (MBD) Is targeting serum phosphate within the normal range recommended for CKD patients? One recent meta-analysis showed that a 1 mg/dL increase in the serum phosphate level was associated with a 29 % increase in all-cause mortality in CKD patients. A sub-analysis using a limited number of well-designed studies with multiple covariates demonstrated an even higher hazardss ratio of 1.35. Due to a lack of evidence, the association of serum phosphate with cardiovascular death in CKD patients remains to be elucidated. In other reports, a high serum phosphate level was associated with a steeper decline in eGFR and an increased risk of ESRD in CKD patients.