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1  with NAFLD as well as in those treated with sevelamer.
2 rol reduction caused by statins and possibly sevelamer.
3 3 by CaCO(3) and decreased even further with sevelamer (16.4 +/- 8.9, P < 0.02 versus CaCO(3)).
4  in contrast, values remained unchanged with sevelamer (9.6 +/- 01 versus 8.9 +/- 0.2 mg/dl; P < 0.00
5                                              Sevelamer, a nonabsorbable hydrogel, is as efficacious a
6                                 Furthermore, sevelamer administration reduced coagulation biomarkers,
7 6 (0.26,0.47) for 100 mg EOS789 plus 1600 mg sevelamer (all not significantly different).
8                                              Sevelamer also exhibits beneficial effects on lipids, co
9                                              Sevelamer also reduced hepatic inflammation and fibrosis
10                         We also analyzed how sevelamer alters inflammation and bile acid signaling in
11 rimental model of CRF, these studies compare sevelamer and calcium carbonate (CaCO(3)) in the control
12 In a head-to-head randomized clinical trial, sevelamer and calcium-based binders achieved similarly e
13     In a randomized clinical trial comparing sevelamer and calcium-based phosphate binders, treatment
14 lar in subjects randomly assigned to receive sevelamer and calcium-based phosphate binders.
15 tatistically significant differences between sevelamer and placebo with regard to LV mass, systolic a
16 ogic explanations for the association (e.g., sevelamer); and (4) drugs that may have resulted in stat
17 ; in this compliant subgroup, treatment with sevelamer associated with lower urinary phosphate excret
18 se report, we explore the unique features of sevelamer-associated recto-sigmoid ulcers which led to h
19 ary artery and aortic calcification, whereas sevelamer attenuated or arrested progression.
20                                              Sevelamer, besides normalizing the serum phosphorus, sur
21 bjects were randomized (292 to FC and 149 to sevelamer carbonate and/or calcium acetate [active contr
22 t2b-deficient mice with the phosphate binder sevelamer carbonate further reduced serum phosphate leve
23 n, this study does not provide evidence that sevelamer carbonate improves LV mass, LV function, or ar
24 ng diabetic and uremic vasculopathy and that sevelamer carbonate may be capable of increasing bone fo
25 duction of established VC by the addition of sevelamer carbonate to the diets of this murine metaboli
26 (2) to calcium acetate, lanthanum carbonate, sevelamer carbonate, or placebo.
27 iod, during which time all patients received sevelamer carbonate, we randomly assigned 109 patients t
28                                     However, sevelamer caused a dramatic reduction of renal Ca deposi
29 eral apposition in Npt2b-deficient mice, but sevelamer did not affect bone formation and rate of mine
30              Thus, in this study population, sevelamer did not reduce microbial translocation but may
31                                              Sevelamer did not significantly change markers of microb
32 e had been treated with the phosphate binder sevelamer for two months.
33 /- 164 pg/ml (P < 0.01) in the CaCO3 and the sevelamer groups, respectively (NS between groups).
34 calcium-containing phosphate binders such as sevelamer have been recommended to reduce cardiovascular
35                                              Sevelamer, however, maintained serum calcium concentrati
36 calcium- and aluminum-free phosphate binder, sevelamer hydrochloride (RenaGel), reduces serum P witho
37                                              Sevelamer hydrochloride is an exchange resin and was not
38 lar permeability, while the BA-binding resin sevelamer hydrochloride protected against CDCA-induced l
39                   In a mouse model of NAFLD, sevelamer improved disease and counteracted innate immun
40 hich may cause inflammation, is decreased by sevelamer in patients undergoing hemodialysis.
41   In this study, we assessed the efficacy of sevelamer in treating mice with non-alcoholic fatty live
42                                              Sevelamer is a nonabsorbed hydrogel that binds phosphoru
43 despite a similar control of serum P and SH, sevelamer is more effective than CaCO(3) in preventing r
44                                              Sevelamer is widely used in chronic kidney disease and e
45                   These results suggest that sevelamer may have important actions in decreasing diabe
46 ort-term and open-label studies suggest that sevelamer might lower the concentration of uric acid, an
47          To what extent the phosphate binder sevelamer modulates these effects is not well understood
48  were randomly assigned to CaCO3 (n = 14) or sevelamer (n = 15), concomitant with either intermittent
49 bonate, we randomly assigned 109 patients to sevelamer (n=55) or placebo (n=54) for an additional 36
50  despite receiving phosphate binder therapy (sevelamer, nonsevelamer, sevelamer plus nonsevelamer, or
51 sis were randomly assigned to receive either sevelamer or calcium-based phosphorus binders in an inte
52 ate binder therapy (sevelamer, nonsevelamer, sevelamer plus nonsevelamer, or multiple nonsevelamer bi
53 rn diet for 12 weeks followed by a diet-plus-sevelamer regimen for 2 or 12 weeks.
54 .1 and 5.6 +/- 0.3 mg/dl (NS) with CaCO3 and sevelamer, respectively.
55         Thus, treatment with either CaCO3 or sevelamer resulted in equivalent control of the biochemi
56 hat treatment with the bile acid sequestrant sevelamer reversed the liver injury and prevented the pr
57  reexamined, and the potential advantages of sevelamer should be considered when selecting a primary
58 urnover renal osteodystrophy; treatment with sevelamer significantly decreased the number of osteocla
59                                              Sevelamer therapy increased osteoblast surfaces in the m
60 tudy, we evaluated the effects of 8 weeks of sevelamer therapy on 36 HIV-infected subjects who were n
61 ion of intestinal BAs by in vivo delivery of sevelamer to WD-fed knockout mice attenuated colonic muc
62                                              Sevelamer-treated NAFLD livers had notably fewer pro-inf
63 nd of the study) was significantly larger in sevelamer-treated subjects (-0.64 mg/dl versus -0.26 mg/
64                      Twenty-three percent of sevelamer-treated subjects experienced a study-related r
65                                              Sevelamer treatment controlled serum P independent of in
66                                              Sevelamer treatment significantly reduced liver steatosi
67                                       During sevelamer treatment, however, levels of soluble tissue f
68 stine of NAFLD mice that was counteracted by sevelamer treatment.
69  (U-HP); UHP + 3% CaCO(3) (U-HP+C); UHP + 3% sevelamer (U-HP+S).
70                                              Sevelamer was as effective as CaCO(3) in the control of
71 cium-based phosphate binders, treatment with sevelamer was associated with a significant reduction in
72                        The phosphorus binder sevelamer was developed to overcome the limitations asso
73                                 In addition, sevelamer was found to be effective in decreasing serum
74 The effects of calcium carbonate (CaCO3) and sevelamer were compared in pediatric peritoneal dialysis
75 IV-infected pigtailed macaques with the drug sevelamer, which binds microbial lipopolysaccharide in t
76 g-term, randomized, clinical trial comparing sevelamer with calcium-based phosphate binders.
77  EOS789 100 mg vs EOS789 100 mg plus 1600 mg sevelamer with meals.
78 this recently-reported entity in patients on sevelamer with suggestive symptoms, as this medication i
79  in serum uric acid concentration induced by sevelamer would be confirmed in a long-term, randomized,