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1 accompanied these renoprotective effects of paricalcitol.
2 roxylase, resulting in increased activity of paricalcitol.
3 secondary hyperparathyroidism received oral paricalcitol 1 mug/d for 3 months, and 8 patients matche
4 conclusion, 52 weeks of treatment with oral paricalcitol (1 mug one time daily) significantly improv
5 ere randomly assigned to receive either oral paricalcitol (1 mug) one time daily (n=30) or matching p
6 ompared the effect of 6-month treatment with paricalcitol (1 mug/d for 3 months and then uptitrated t
7 atment of the diabetic mice with losartan or paricalcitol (19-nor-1,25-dihydroxyvitamin D(2), an acti
10 ril (30 mg/L in drinking water; E), uremic + paricalcitol (19-nor; 0.8 microg/kg, three times a week)
11 cipients were randomized 1:1 to receive oral paricalcitol, 2 mug per day, for the first year posttran
12 pants were randomly assigned to receive oral paricalcitol, 2 mug/d (n =115), or matching placebo (n =
14 alysis who started to receive treatment with paricalcitol (29,021 patients) or calcitriol (38,378 pat
18 omatin immunoprecipitation assay showed that paricalcitol abolished the binding of p65 to its cognate
21 S induction depended on NF-kappaB signaling, paricalcitol affected neither TNF-alpha-mediated IkappaB
25 ARalpha in PR9 cells, and the combination of paricalcitol and As2O3 enhanced their monocytic differen
28 ns retrieved, six studies (four studies with paricalcitol and two studies with calcitriol) providing
29 -ray absorption, significantly improved with paricalcitol at 6 months (P<0.05 for both densities).
30 obably by increasing intracellular levels of paricalcitol by decreasing the function of the mitochond
31 owever, combined treatment with losartan and paricalcitol completely prevented albuminuria, restored
32 sues, we tested whether the vitamin D analog paricalcitol could ameliorate podocyte injury, proteinur
39 oid hormone levels significantly declined on paricalcitol from 115.6 (94.8-152.0) to 63.3 (52.0-79.7)
41 olic lateral mitral annular tissue velocity (paricalcitol group, -0.01 cm/s [95% CI, -0.63 to 0.60 cm
42 dex did not differ between treatment groups (paricalcitol group, 0.34 g/m(2.7) [95% CI, -0.14 to 0.83
43 y 6.7 and 11.9 percent, respectively, in the paricalcitol group, as compared with 8.2 and 13.9 percen
47 ng-term studies are needed to assess whether paricalcitol-induced increase in KLOTHO gene expression
48 ic blockade of Wnt/beta-catenin signaling by paricalcitol inhibited MMP-7 expression in diseased kidn
49 a human proximal tubular cell line (HKC-8), paricalcitol inhibited RANTES mRNA and protein expressio
55 epithelial cells, accompanied renal injury; paricalcitol largely abolished this induction of renal b
57 linically relevant dosages of calcitriol and paricalcitol may protect against CKD-stimulated vascular
58 effects of the VDR activators calcitriol and paricalcitol on aortic calcification in a mouse model of
59 -concept study aimed to assess the effect of paricalcitol on fibroblast growth factor-23/KLOTHO axis
61 e effect of the synthetic vitamin D analogue paricalcitol on renal inflammation was investigated in a
64 effects of the vitamin D receptor activator paricalcitol (PARI) and dietary sodium restriction on re
68 O3 increased the transcriptional activity of paricalcitol probably by increasing intracellular levels
72 pared with vehicle-treated proteinuric rats, paricalcitol showed markedly reduced renal lymphangiogen
74 adynamic bone disorder; both calcitriol and paricalcitol stimulated osteoblast surfaces and rates of
78 atients who received 12 wk of treatment with paricalcitol, the levels of iPTH decreased significantly
79 d assessed changes after cholecalciferol and paricalcitol therapies in both vitamin D-responsive prot
80 ine phosphatase and osteocalcin decreased on paricalcitol therapy only and significantly differed bet
84 lood mononuclear cells increased by 45.7% in paricalcitol-treated patients (P < 0.01), without change
86 confidence interval, 10 to 21 percent) among paricalcitol-treated patients than among calcitriol-trea
92 p65 formed a complex in tubular cells after paricalcitol treatment, which inhibited the ability of p
93 le range], -2.59 [-6.13 to 0.32] g/m(2) with paricalcitol versus -4.85 [-9.89 to 1.10] g/m(2) with pl
94 The mortality rate among patients receiving paricalcitol was 3417 per 19,031 person-years (0.180 per
95 ong patients who switched from calcitriol to paricalcitol was 73 percent, as compared with 64 percent
98 econdary hyperparathyroidism, calcitriol and paricalcitol were protective against aortic calcificatio
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