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1 in wild-type and Fgf23(-/-) mice, it reduces serum phosphate.
2 rats over 8 hours increased FEPi, decreased serum phosphate (1.95 +/- 0.1 to 1.53 +/- 0.09 mmol/l, P
3 FGF23 neutralization significantly increased serum phosphate, 1,25(OH)2D and BUN, and decreased serum
4 we randomly assigned 162 eligible patients (serum phosphate =6.0 to <10.0 mg/dl and a 1.5-mg/dl incr
6 this commentary touches on patients with low serum phosphate after acute hospitalization, those with
7 analysis of race, socioeconomic status, and serum phosphate among 2879 participants in the Chronic R
9 ar calcification is due, in part, to reduced serum phosphate, an important inducer of VSMC-mediated v
10 ing levels of FGF23, exhibited low levels of serum phosphate and 1,25(OH)(2)D, reduced expression of
11 ion, we observed dose-dependent increases in serum phosphate and aortic calcification associated with
14 ven the association between higher levels of serum phosphate and cardiovascular disease, further stud
15 esents a novel therapeutic approach to lower serum phosphate and FGF23 levels that will be tested in
18 rt independent associations between elevated serum phosphate and fibroblast growth factor 23 (FGF23)
19 measures of phosphorus metabolism, including serum phosphate and parathyroid hormone (PTH) levels, di
22 ctors are integrated to yield the measurable serum phosphate are only now beginning to be studied.
24 dietary phosphorus intake to mild changes in serum phosphate because of the nature of the study desig
26 rtial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skelet
29 6], p<0.001); this effect was independent of serum phosphate concentration but associated with urinar
30 The primary efficacy end point was change in serum phosphate concentration from baseline (randomizati
32 d trial assessed the effects of tenapanor on serum phosphate concentration in patients with hyperphos
34 In multivariate Cox regression analysis, serum phosphate concentration remained a statistically s
36 and estimated GFR, each 1-mg/dl increment in serum phosphate concentration was associated with a 21%
40 ry end points were serum iPTH concentration, serum phosphate concentration, bone mineral density, vas
41 biosensor is also suitable to determine the serum phosphate concentration, with a recovery of 86-104
47 ly significant, dose-dependent reductions in serum phosphate concentrations in patients with hyperpho
49 st incomes or who were unemployed had higher serum phosphate concentrations than participants with th
55 lities and are independently associated with serum phosphate, Fe(PO4), and calcitriol deficiency.
56 2% to 2.2 +/- 1.1% (P < 0.05), and increased serum phosphate from 2.9 +/- 0.2 mg/dl to 4.1 +/- 0.2 mg
62 notype of predialysis kidney disease: normal serum phosphate, increased fractional excretion of phosp
64 rum calcification propensity included higher serum phosphate, ionized calcium, increased bone osteocl
65 ve study are the first to show that a higher serum phosphate is a predictor of mortality in patients
67 and the mechanism by which the elevation of serum phosphate is thought to induce hypocalcemia is dis
68 phosphate excretion and serum FGF-23 but not serum phosphate, klotho, vitamin D, or cardiovascular-re
69 apanor provided dose-dependent reductions in serum phosphate level from baseline (least squares mean
71 study was to investigate whether an elevated serum phosphate level was an independent predictor of mo
72 Patients in the low-phosphate group (median serum phosphate level, 2.0 mg per deciliter [0.6 mmol pe
73 ent PHEX protein/enzyme leads to a decreased serum phosphate level, which cause mineralization defect
76 m magnesium levels (P = 1.2 * 10(-3)), lower serum phosphate levels (P = 2.8 * 10(-7)) and lower bone
79 n uremic patients, is highly correlated with serum phosphate levels and cardiovascular mortality.
80 s were independent of baseline and follow-up serum phosphate levels and persisted in analyses that ex
81 n = 3186) patients matched by their baseline serum phosphate levels and propensity score of receiving
83 Although we also observed differences in serum phosphate levels by race, income modified this rel
87 FGF-23 may contribute to maintaining normal serum phosphate levels in the face of advancing CKD but
89 , and although elevated FGF23 helps maintain serum phosphate levels in the normal range in CKD, it ma
93 osphate levels and 8 patients who had normal serum phosphate levels, all of whom were receiving imati
94 -)/klotho(-/-) mice are viable and have high serum phosphate levels, similar to Fgf23(-/-) and klotho
95 erestingly, the null mice also displayed low serum phosphate levels, while calcium levels remained un
101 nction declines; is linearly associated with serum phosphate levels; is associated with increased pho
102 tudies will need to determine whether excess serum phosphate may explain disparities in kidney diseas
103 were available for analysis, and 3490 had a serum phosphate measurement during the previous 18 mo.
105 comp/hom and het individuals with decreased serum phosphate (odds ratio [OR], 0.75, 95% confidence i
107 n were studied prospectively with respect to serum phosphate, phosphate requirements, as well as rena
108 nts with a renal transplant and suggest that serum phosphate provides additional, independent, progno
112 cular, and biochemical covariates, including serum phosphate, risk of death among patients in the low
113 , estimated GFR, albuminuria, serum calcium, serum phosphate, serum bicarbonate, and serum albumin (C
114 onship: Blacks had 0.11 to 0.13 mg/dl higher serum phosphate than whites in the highest income groups
117 tho(-/-) and klotho(-/-) mice does not lower serum phosphate, whereas in wild-type and Fgf23(-/-) mic
118 ogic studies suggest that mild elevations of serum phosphate within the normal range are associated w
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