ライフサイエンスコーパス: serum phosphate

1 in wild-type and Fgf23(-/-) mice, it reduces serum phosphate.

2 standard of care, which typically normalizes serum phosphate.

3 for eGFR and age, but not when adjusted for serum phosphate.

4 rats over 8 hours increased FEPi, decreased serum phosphate (1.95 +/- 0.1 to 1.53 +/- 0.09 mmol/l, P

5 FGF23 neutralization significantly increased serum phosphate, 1,25(OH)2D and BUN, and decreased serum

6 , noncalcium-based phosphate binders reduced serum phosphate (12 trials, weighted mean difference -0.

7 we randomly assigned 162 eligible patients (serum phosphate =6.0 to <10.0 mg/dl and a 1.5-mg/dl incr

8 Dose-dependent elevations in serum phosphate, a manifestation of pharmacodynamic effe

9 this commentary touches on patients with low serum phosphate after acute hospitalization, those with

10 An elevation in serum phosphate-also called hyperphosphatemia-is associa

11 analysis of race, socioeconomic status, and serum phosphate among 2879 participants in the Chronic R

12 The regulation of serum phosphate, an acknowledged risk factor for chronic

13 ar calcification is due, in part, to reduced serum phosphate, an important inducer of VSMC-mediated v

14 ing levels of FGF23, exhibited low levels of serum phosphate and 1,25(OH)(2)D, reduced expression of

15 pounds blocked FGF23 signaling and increased serum phosphate and 1,25-dihydroxyvitamin D [1,25(OH)(2)

16 Serum phosphate and 12 additional biomarkers of mineral

17 ion, we observed dose-dependent increases in serum phosphate and aortic calcification associated with

18 remic mice had significantly lower levels of serum phosphate and attenuation of FGF23.

19 Whereas serum phosphate and calcium levels declined to normal by

20 ven the association between higher levels of serum phosphate and cardiovascular disease, further stud

21 of active intestinal phosphate transport) on serum phosphate and FGF23 in stage 3b/4 CKD, we conducte

22 esents a novel therapeutic approach to lower serum phosphate and FGF23 levels that will be tested in

23 may reduce dietary phosphate absorption and serum phosphate and FGF23 levels.

24 absorption is one modifiable determinant of serum phosphate and FGF23 levels.

25 rt independent associations between elevated serum phosphate and fibroblast growth factor 23 (FGF23)

26 Higher serum phosphate and fibroblast growth factor-23 (FGF23)

27 ce under normal conditions, resulting in low serum phosphate and fibroblast growth factor-23 (FGF23)

28 serum ferritin, and it significantly reduced serum phosphate and intact FGF23 (P<0.001 for all).

29 mary end points were change from baseline in serum phosphate and intact FGF23 concentrations.

30 Elevated serum phosphate and parathyroid hormone (PTH) concentrat

31 measures of phosphorus metabolism, including serum phosphate and parathyroid hormone (PTH) levels, di

32 Normal serum phosphate and parathyroid hormone were observed in

33 treatment start time) may be associated with serum phosphate and PTH concentrations.

34 ium-based phosphate-lowering therapy reduced serum phosphate and urinary phosphate excretion, but the

35 ures of calcium homeostasis, except elevated serum phosphate and urine calcium levels in girls.

36 The loss of Scribble impacted serum phosphate and vitamin D levels and caused signific

37 controlling metabolic processes ranging from serum phosphate and vitamin D levels to glucose uptake,

38 rowth factor 23 receptor complex to regulate serum phosphate and vitamin D levels.

39 ctors are integrated to yield the measurable serum phosphate are only now beginning to be studied.

40 Associations between serum phosphate, arterial stiffness, and left ventricula

41 Our primary outcome was serum phosphate at 24 hours with a noninferiority margin

42 dietary phosphorus intake to mild changes in serum phosphate because of the nature of the study desig

43 Owing to an imbalance in baseline serum phosphate between groups, raising concern for bias

44 stages 3-5 have shown only modest changes in serum phosphate but evaluated morning phosphate.

45 rtial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skelet

46 Ablation of FGF23 results in elevated serum phosphate, calcium, and 1,25-dihydroxyvitamin D3 [

47 Serum phosphate, calcium, and fibroblast growth factor 2

48 6], p<0.001); this effect was independent of serum phosphate concentration but associated with urinar

49 The primary efficacy end point was change in serum phosphate concentration from baseline (randomizati

50 of renal calcium and phosphate and increased serum phosphate concentration in gsk3(KI) mice.

51 d trial assessed the effects of tenapanor on serum phosphate concentration in patients with hyperphos

52 Normalization of serum phosphate concentration occurred in almost all pat

53 In multivariate Cox regression analysis, serum phosphate concentration remained a statistically s

54 The mean serum phosphate concentration was 5.2+/-1.5 mg/dl, and t

55 In Kaplan-Meier analysis, serum phosphate concentration was a significant predicto

56 and estimated GFR, each 1-mg/dl increment in serum phosphate concentration was associated with a 21%

57 Each 0.5 mg/dl higher serum phosphate concentration was associated with greate

58 The serum phosphate concentration was higher in the postmeno

59 Serum phosphate concentration was significantly associat

60 At 24 hours, mean ( sd ) serum phosphate concentration were enteral 0.89 mmol/L (

61 ry end points were serum iPTH concentration, serum phosphate concentration, bone mineral density, vas

62 biosensor is also suitable to determine the serum phosphate concentration, with a recovery of 86-104

63 variability was explained by age, LVMI, and serum phosphate concentration.

64 osphate excretion, leading to an increase in serum phosphate concentration.

65 As expected, ferric citrate lowered serum phosphate concentrations and increased serum iron

66 Within the normal range, higher serum phosphate concentrations are associated with cardi

67 Mean serum phosphate concentrations at baseline (after washou

68 We determined the circadian pattern of serum phosphate concentrations in CKD and whether it was

69 ly significant, dose-dependent reductions in serum phosphate concentrations in patients with hyperpho

70 socioeconomic status associates with higher serum phosphate concentrations irrespective of race.

71 st incomes or who were unemployed had higher serum phosphate concentrations than participants with th

72 Current guidelines recommend lowering serum phosphate concentrations toward normal.

73 Serum phosphate concentrations were within the normal ra

74 We examined associations of serum phosphate concentrations with vascular and valvula

75 In conclusion, higher serum phosphate concentrations, although still within th

76 are not always associated with increases in serum phosphate concentrations.

77 CRD mice had significantly higher serum phosphate, creatinine, and cystatin C levels than

78 Overall, serum phosphate declined by a mean of 36% at Day 7, with

79 ulation of phosphate occurs independently of serum phosphate elevations and is not necessarily accomp

80 y calcifications and occurs independently of serum phosphate elevations.

81 While there were no changes in serum phosphate, FC reduced C-terminal fibroblast growth

82 lities and are independently associated with serum phosphate, Fe(PO4), and calcitriol deficiency.

83 y of patients with and without IBD evaluated serum phosphate for 28 days following intravenous FCM, a

84 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

85 278 participants with stage 3b or 4 CKD and serum phosphate >1.00 mmol/L (3.10 mg/dl) to 500 mg lant

86 In fully adjusted models, serum phosphate had a nadir at 11:00 am of 4.97 (IQR, 4.

87 High serum phosphate has been identified as an important cont

88 The effects of these factors on serum phosphate have major implications for what is unde

89 rs may be a therapeutic approach to modulate serum phosphate in CKD.

90 vents and mortality strongly correlates with serum phosphate in individuals with CKD.

91 Guidelines recommend reducing elevated serum phosphate in patients with CKD.

92 Tenapanor significantly reduced elevated serum phosphate in patients with hyperphosphatemia recei

93 t range (8.4-10.2 mg/dl), 41.5% patients had serum phosphate in target range (3.5-5.5 mg/dl) and 51.2

94 disordered skeletal modeling, also reducing serum phosphate in the process.

95 tion (P >= 0.20), whereas serum chloride and serum phosphate increased significantly under AA (both P

96 notype of predialysis kidney disease: normal serum phosphate, increased fractional excretion of phosp

97 Serum phosphate independently predicts cardiovascular mo

98 rum calcification propensity included higher serum phosphate, ionized calcium, increased bone osteocl

99 ve study are the first to show that a higher serum phosphate is a predictor of mortality in patients

100 A circadian pattern of serum phosphate is observed in CKD with lowest concentra

101 and the mechanism by which the elevation of serum phosphate is thought to induce hypocalcemia is dis

102 phosphate excretion and serum FGF-23 but not serum phosphate, klotho, vitamin D, or cardiovascular-re

103 point was the incidence of hypophosphatemia (serum phosphate level <2.0 mg/dL) between baseline and d

104 The serum phosphate level (5.83 +/- 0.90 vs. 5.84 +/- 1.04 m

105 apanor provided dose-dependent reductions in serum phosphate level from baseline (least squares mean

106 anced, the factors determining regulation of serum phosphate level remain enigmatic.

107 study was to investigate whether an elevated serum phosphate level was an independent predictor of mo

108 Patients in the low-phosphate group (median serum phosphate level, 2.0 mg per deciliter [0.6 mmol pe

109 ent PHEX protein/enzyme leads to a decreased serum phosphate level, which cause mineralization defect

110 en identified as significant contributors to serum phosphate level.

111 After adjustment, serum phosphate levels >3.5 mg/dl were associated with a

112 It is known that high serum phosphate levels (hyperphosphatemia) cause vascula

113 m magnesium levels (P = 1.2 * 10(-3)), lower serum phosphate levels (P = 2.8 * 10(-7)) and lower bone

114 U/HP group, and no differences were noted in serum phosphate levels among groups.

115 We identified 16 patients who had low serum phosphate levels and 8 patients who had normal ser

116 n uremic patients, is highly correlated with serum phosphate levels and cardiovascular mortality.

117 s were independent of baseline and follow-up serum phosphate levels and persisted in analyses that ex

118 n = 3186) patients matched by their baseline serum phosphate levels and propensity score of receiving

119 In patients on hemodialysis, elevated serum phosphate levels are an independent predictor of m

120 Although we also observed differences in serum phosphate levels by race, income modified this rel

121 Furthermore, CKD patients with higher serum phosphate levels expressed more FGF23 in skeletal

122 Elevated serum phosphate levels have been linked with vascular ca

123 We examined mortality according to serum phosphate levels in a prospective cohort of 10,044

124 Serum phosphate levels in KL (-/-) mice were kept in the

125 Genetically reducing serum phosphate levels in klotho(-/-) mice by generating

126 FGF-23 may contribute to maintaining normal serum phosphate levels in the face of advancing CKD but

127 Serum phosphate levels in the highest quartile (>5.5 mg

128 , and although elevated FGF23 helps maintain serum phosphate levels in the normal range in CKD, it ma

129 We measured serum phosphate levels over the course of the trial.

130 ld be achieved with no significant effect on serum phosphate levels relative to vehicle.

131 Elevated serum phosphate levels were independently associated wit

132 Serum phosphate levels were lower in dialysis patients u

133 Fgf23 KO mice had elevated serum phosphate levels when administered a high-phosphat

134 Higher serum phosphate levels within the normal range were asso

135 reased urinary phosphate excretion maintains serum phosphate levels within the normal range, thus pro

136 osphate levels and 8 patients who had normal serum phosphate levels, all of whom were receiving imati

137 ventions maintained normocalcemia, increased serum phosphate levels, and improved dentoalveolar miner

138 -)/klotho(-/-) mice are viable and have high serum phosphate levels, similar to Fgf23(-/-) and klotho

139 erestingly, the null mice also displayed low serum phosphate levels, while calcium levels remained un

140 ients with chronic kidney disease and normal serum phosphate levels.

141 nd resorption), even in patients with normal serum phosphate levels.

142 y with each subsequent 0.5-mg/dl increase in serum phosphate levels.

143 renal proximal tubules and thereby regulate serum phosphate levels.

144 was not accompanied by further elevations in serum phosphate levels.

145 -deficient mice or alphaKL-null mice reduced serum phosphate levels.

146 e binder sevelamer carbonate further reduced serum phosphate levels.

147 nction declines; is linearly associated with serum phosphate levels; is associated with increased pho

148 eloped moderate to severe hypophosphataemia (serum phosphate < 0.6 mmol/L).

149 Serum phosphate < 1.05 mmol/L on Day 2 predicted suscept

150 tudies will need to determine whether excess serum phosphate may explain disparities in kidney diseas

151 were available for analysis, and 3490 had a serum phosphate measurement during the previous 18 mo.

152 In contrast, neither the serum phosphate nor 1,25(OH)(2)D levels were altered in

153 comp/hom and het individuals with decreased serum phosphate (odds ratio [OR], 0.75, 95% confidence i

154 or NAM treatment did not significantly lower serum phosphate or FGF23 in stage 3b/4 CKD over 12 month

155 The primary end point was mean change in serum phosphate over the 4-week withdrawal period for th

156 (p < 0.001), male sex (p < 0.01), and higher serum phosphate (p < 0.001).

157 l density (BMD), osteomalacia, and decreased serum phosphate (P(i)).

158 ups, nor did abdominal aortic calcification, serum phosphate, parathyroid hormone, FGF23, and 24-hour

159 n were studied prospectively with respect to serum phosphate, phosphate requirements, as well as rena

160 nts with a renal transplant and suggest that serum phosphate provides additional, independent, progno

161 The values of age, serum phosphate, pulse wave velocity, left ventricular m

162 ps experienced significant decreases in mean serum phosphate (reductions of 1.00, 1.02, and 1.19 mg/d

163 The physiology of serum phosphate regulation and the mechanism by which th

164 hosphate excretion and hypophosphaturia, but serum phosphate remained unchanged.

165 cular, and biochemical covariates, including serum phosphate, risk of death among patients in the low

166 , estimated GFR, albuminuria, serum calcium, serum phosphate, serum bicarbonate, and serum albumin (C

167 domized trial compared a higher versus lower serum phosphate target in patients undergoing maintenanc

168 Serum phosphate targets in maintenance hemodialysis are

169 The Pragmatic Trial of Higher versus Lower Serum Phosphate Targets in Patients Undergoing Hemodialy

170 onship: Blacks had 0.11 to 0.13 mg/dl higher serum phosphate than whites in the highest income groups

171 gous carriers is intermediate with decreased serum phosphate, tubular reabsorption of phosphate (TRP

172 Mean serum phosphate was 1.25 mmol/L (3.87 mg/dl), mean pulse

173 At baseline, serum phosphate was 3.7 mg/dl and median FGF23 was 99 pg

174 Serum phosphate was measured at baseline and prospective

175 Serum phosphate was significantly higher in those renal

176 tho(-/-) and klotho(-/-) mice does not lower serum phosphate, whereas in wild-type and Fgf23(-/-) mic

177 ogic studies suggest that mild elevations of serum phosphate within the normal range are associated w