ライフサイエンスコーパス: serum sodium

1 hyponatremia or the absolute decrease in the serum sodium.

2 from those incurred by patients with normal serum sodium.

3 , hypertension, diabetes, smoking status and serum sodium.

4 d low ejection fraction, blood pressure, and serum sodium.

5 ingdom is now based on a model that includes serum sodium.

6 nsity lipoprotein cholesterol by 20%, raised serum sodium (0.44+/-0.14 mmol/L, P=0.02), and lowered s

7 ], 1.01 to 1.12); for a 2 mmol/l decrease in serum sodium, 1.22 (95% CI, 1.08 to 1.38); and for a 10

8 Serum sodium (128 +/- 4 vs. 138 +/- 1 mmol/L, p <.05) an

9 asures, except OMT patients had a lower mean serum sodium (128 mg/dl vs. 134 mg/dl; p = 0.001) and a

10 +/- 12 versus 83 +/- 14 mmHg, P = 0.009) and serum sodium (131 +/- 7 versus 135 +/- 5 mEq/L, P = 0.00

11 del for Endstage Liver Disease (MELD) score, serum sodium, albumin, lactulose use, rifaximin use, and

12 The absolute change in serum sodium alone is a poor predictor of clinical sympt

13 Model for End-Stage Liver Disease including serum sodium and Child Pugh Scores.

14 death specific to progressive HF were SDNN, serum sodium and creatinine levels.

15 We found that, after the water load, serum sodium and free water clearance were diminished in

16 he water load resulted in a reduction of the serum sodium and free water clearance without a concomit

17 liver disease - sodium (MELDNa) incorporates serum sodium and has been shown to improve the predictiv

18 normal-to-normal RR intervals (SDNN); lower serum sodium and higher creatinine levels; higher cardio

19 viral therapy, chief complaint of fever, low serum sodium and low hemoglobin.

20 Torcetrapib raised serum sodium and lowered potassium, consistent with an a

21 The median serum sodium and MELD scores were 137 mEq/L (range, 110-

22 Lower serum sodium and more red blood cell transfusions were a

23 with a MELD score of less than 21, only low serum sodium and persistent ascites were independent pre

24 In ambulant outpatients with chronic HF, low serum sodium and SDNN and high serum creatinine identify

25 estigated the relationship between admission serum sodium and the primary end point of days hospitali

26 ebrospinal fluid volume, ventricular volume, serum sodium, and Glasgow Coma Scale scores were assesse

27 ology, LV systolic function, renal function, serum sodium, and PAP.

28 rence, alphafetoprotein at recurrence, donor serum sodium, and pretransplant recipient neutrophil-lym

29 Disorders of serum sodium are both the most common and probably most

30 questions: Which of the determinants of the serum sodium are deranged and what is the underlying cul

31 sociated with low serum sodium, we evaluated serum sodium as an independent predictor of mortality in

32 id therapy and fluid losses on the patient's serum sodium, balances potential benefits and risks, and

33 of End Stage Liver Disease score (MELD), and serum sodium based modifications like the MELD-Na score

34 emporal progression of clinical features and serum sodium, brain magnetic resonance imaging (MRI), po

35 in AHF (signs of cerebral hypoperfusion, low serum sodium, chronic obstructive pulmonary disease, and

36 entration <135 mmol/L and hypernatremia as a serum sodium concentration >145 mmol/L.

37 sodium concentration and with hyponatremia (serum sodium concentration < or =135 mEq/L) in 2 non-His

38 Hyponatremia was defined as a serum sodium concentration <135 mmol/L and hypernatremia

39 complications, especially if the decrease in serum sodium concentration ([Na+]) is large or rapid.

40 e patients 12 months after LT (P=0.04), with serum sodium concentration (P=0.01) predictive for graft

41 A strong association between change in serum sodium concentration and change in VBR was noted a

42 olymorphism is significantly associated with serum sodium concentration and with hyponatremia (serum

43 wide study shows that the MELD score and the serum sodium concentration are important predictors of s

44 LD point and 1.05 per 1-unit decrease in the serum sodium concentration for values between 125 and 14

45 e average daily area under the curve for the serum sodium concentration from baseline to day 4 and th

46 Vasopressin antagonists increase the serum sodium concentration in patients who have euvolemi

47 aucasian male populations; in addition, mean serum sodium concentration is lower among subjects with

48 ccording to the MELD score combined with the serum sodium concentration might have resulted in transp

49 Thirteen percent had hyponatremia (a serum sodium concentration of 135 mmol per liter or less

50 1 M NaCl to induce a 25 to 28 mM increase in serum sodium concentration over 200 min or an infusate t

51 ay be continued at rates of 2/1/0.5 ml/kg/h; serum sodium concentration should be measured periodical

52 An increase in serum sodium concentration significantly decreases ICP a

53 Fluctuation in serum sodium concentration was also independently associ

54 t, the combination of the MELD score and the serum sodium concentration was considerably higher than

55 entration, indicating that the effect of the serum sodium concentration was greater in patients with

56 t 12 hrs correlating with an increase in the serum sodium concentration was observed in patients with

57 Both the MELD score and the serum sodium concentration were significantly associated

58 We examined the association of serum sodium concentration with all-cause mortality in a

59 ronic kidney disease, but the association of serum sodium concentration with mortality in such patien

60 Hyponatremia (serum sodium concentration, <135 mmol per liter) is a pr

61 ion was found between the MELD score and the serum sodium concentration, indicating that the effect o

62 ) score with and without the addition of the serum sodium concentration.

63 aline administration may further depress the serum sodium concentration.

64 over 200 min or an infusate that maintained serum sodium concentration.

65 reflected clinically as abnormalities in the serum sodium concentration.

66 th an aquaresis that leads to an increase in serum sodium concentration.

67 ptor antagonist, was effective in increasing serum sodium concentrations at day 4 and day 30.

68 Serum sodium concentrations increased more in the tolvap

69 Serum sodium concentrations obtained immediately prior t

70 quisition of dysnatremia and fluctuations in serum sodium concentrations on hospital mortality in the

71 Serum sodium concentrations significantly predicted mort

72 us infusion of 3% saline/acetate to increase serum sodium concentrations to 145 to 155 mmol/L.

73 Fluctuations in serum sodium concentrations were independently associate

74 Despite similar serum sodium concentrations, clinical manifestations can

75 daily sodium and fluid intake, weight loss, serum sodium concentrations, gender, gestational age, pn

76 We monitored continuously mean ICP, serum sodium concentrations, mean arterial pressure, cer

77 arterial pressure, central venous pressure, serum sodium concentrations, serum osmolarity, and serum

78 o 60 mg daily, if necessary, on the basis of serum sodium concentrations.

79 nic saline is an effective agent to increase serum sodium concentrations.

80 Hemodynamics, inotrope score, and serum sodium did not differ between groups at any time p

81 Pre-OLT serum sodium does not have a statistically significant i

82 ed at outpatient week 1, but body weight and serum sodium effects persisted long after discharge.

83 The increase in serum sodium exceeded the desired 1 mmol/L per h at init

84 c significance of persistent ascites and low serum sodium for low MELD score patients was confirmed i

85 and ischemia times for the peak or terminal serum sodium groups.

86 m AST/ALT >500, maximum bilirubin >2.0, peak serum sodium >170, HBV/HCV/HTLV reactive, donation after

87 of 2,175 subjects, 1,495 (68.7%) had normal serum sodium (>135 mEq/L) at OLT, whereas mild hyponatre

88 Serum sodium had no impact on survival up to 90 days aft

89 pressure (HR 0.98, 95% CI 0.97 to 0.99), and serum sodium (HR 0.93, 95% CI 0.90 to 0.96).

90 In conclusion, persistent ascites and low serum sodium identify patients with cirrhosis with high

91 luding points for persistent ascites and low serum sodium, improved prediction of early pretransplant

92 The prognostic value of serum sodium in ADHF was diminished compared with chlori

93 Incorporation of serum sodium in organ allocation may not adversely affec

94 The prognostic value of serum sodium in patients hospitalized for worsening hear

95 A decrease in edema and a normalization of serum sodium in patients with hyponatremia were observed

96 reduced body weight and edema and normalized serum sodium in the hyponatremic patients.

97 not differ importantly, for peak or terminal serum sodium, in posttransplant alanine aminotransferase

98 Serum sodium increase was associated with increase in to

99 Mean serum sodium increased from 130.8 mmol/L at baseline to

100 er, laboratory variation and manipulation of serum sodium is a concern.

101 lized for worsening heart failure, admission serum sodium is an independent predictor of increased nu

102 infarction (AOR 1.59, 95% CI 1.17, 2.16), a serum sodium less than 133 on admission (AOR 1.96, 95% C

103 rs of the time to death were age (older) and serum sodium level (lower), irrespective of the serum cT

104 The primary outcome was mean serum sodium level at 48 hours.

105 An abnormal serum sodium level is the most common electrolyte disord

106 These results suggest that donor serum sodium level likely has little clinical impact on

107 HAH was defined as development of a serum sodium level of </=135 mEq/L during hospitalizatio

108 a sliding scale was used to achieve a target serum sodium level that would maintain ICP <20 mm Hg onc

109 The association of serum sodium level with mortality was U-shaped, with the

110 ft ventricular (LV) systolic function, lower serum sodium level, and older age.

111 ent, the incidence of CPM did correlate with serum sodium levels (P < 0.01).

112 ariate analysis showed that low preoperative serum sodium levels (P = 0.012), histological cirrhosis

113 (P < 0.001, HR = 9.83, 95% CI = 4.51-21.45), serum sodium levels (P = 0.03, HR = 0.96, 95% CI = 0.92-

114 eteriorated in the hospital had decreases in serum sodium levels (P=0.007), and increases in body tem

115 The importance of serum sodium levels and the presence of ascites in the p

116 The presence of ascites and serum sodium levels are important variables associated w

117 Both lower and higher serum sodium levels are independently associated with hi

118 The direct medical costs of abnormal serum sodium levels are not well understood.

119 Serum sodium levels became significantly different from

120 ich oxcarbazepine can lead to a reduction of serum sodium levels could have therapeutic implications

121 ange upper and lower bounds, and incorporate serum sodium levels improved wait-list mortality predict

122 graft rejection, despite similar mean BP and serum sodium levels in HSD and normal salt diet (NSD) gr

123 ance of serum chloride levels in relation to serum sodium levels in patients with ADHF.

124 Patients with serum sodium levels of <130, 130 to 135.9, 145.1 to 150,

125 rtonic saline (30%) via infusion to maintain serum sodium levels of 145-155 mmol/L.

126 In patients with hyponatremia, serum sodium levels significantly increased.

127 Both peak and terminal serum sodium levels were categorized as (1) severe for a

128 , 1 month to 18 years), with normal baseline serum sodium levels who were anticipated to require intr

129 um <135 mmol/L), 162,829 (97.3%) with normal serum sodium levels, and 3196 (1.9%) with hypernatremia

130 wever, ETx stimulated early diuresis,reduced serum sodium levels, and had more pronounced vasodilator

131 concentrated on the clinical significance of serum sodium levels.

132 ignificantly based on peak or terminal donor serum sodium levels.

133 f MELD and 2 modifications (MELDNa [includes serum sodium levels] and MELD-XI [does not include inter

134 Serum sodium (lower) was an independent predictor of all

135 In conclusion, serum sodium <126 mEq/L at listing or while listed for t

136 The risk of death with serum sodium <126 mEq/L at listing or while listed was i

137 ogen >/=30 mg/dL (OR, 1.5; 95% CI, 1.1-2.2), serum sodium <130 mmol/L (OR, 1.8; 95% CI, 1.02-3.1), he

138 were 1274 patients (0.8%) with hyponatremia (serum sodium <135 mmol/L), 162,829 (97.3%) with normal s

139 e symptoms, diabetes mellitus, lung disease, serum sodium <140 mEq/L, atrial fibrillation or flutter,

140 MELD score, persistent ascites, and low serum sodium (<135 meq/L) were independent predictors of

141 s not on dialysis, ln albumin, ln bilirubin, serum sodium<134 mEq/L, status-1, previous LT, transjugu

142 cerebral demyelination are correction of the serum sodium more than 25 mEq/L in the first 48 hours of

143 The serum sodium/myo-inositol cotransporter gene is located

144 Serum sodium (Na) concentrations have been suggested as

145 Inclusion of serum sodium (Na) into the MELD score was found to impro

146 Decreasing preoperative serum sodium (odds ratio, 1.41; 95% confidence interval,

147 ox proportional hazards analysis showed that serum sodium on admission, when modeled linearly, predic

148 ition and fluid rate to prevent disorders in serum sodium or volume status from occurring.

149 0.001) with no incremental contribution from serum sodium (P=0.49).

150 U increase (HR: 1.22, 95% CI: 0.96 to 1.55), serum sodium, per unit increase (HR: 0.93, 95% CI: 0.87

151 serial measurements of serum osmolality and serum sodium, plasma arginine vasopressin (AVP), and pla

152 Serum sodium, potassium, and chloride concentrations; se

153 correlated with hemoglobin, hematocrit, and serum sodium, potassium, creatinine, and osmolality.

154 Stage Liver Disease score, Child-Pugh score, serum sodium, previous variceal bleeding, cirrhosis etio

155 Accordingly, serum sodium should be maintained at least within high n

156 However, the total change in serum sodium should not exceed 5 mEq/L in the initial 1-

157 Risk in Communities Study demonstrated that serum sodium significantly contributes to prediction of

158 cts of VRA are rare, and the rate of rise in serum sodium that they produce seems unlikely to lead to

159 infusion of 3% hypertonic saline to increase serum sodium to levels necessary to reduce ICP < or =20

160 Addition of serum sodium to MELD increases the ability to predict 3-

161 transplantation and whether the addition of serum sodium to MELD was superior to MELD alone.

162 , peripheral edema, systolic blood pressure, serum sodium, urea, creatinine, and albumin) performed s

163 L during hospitalization in the setting of a serum sodium value >135 mEq/L on admission.

164 CAH was defined as a serum sodium value of </=135 mEq/L at the time of hospit

165 There was a steady increase in serum sodium versus time zero that reached statistical s

166 107 mm Hg in those not receiving inotropes, serum sodium was 134 versus 137 mEq/L, and left ventricu

167 The mean highest serum sodium was 170.7 mEq/L (range, 157-187 mEq/L).

168 Lower serum sodium was associated with higher in-hospital and

169 Serum sodium was measured, serum osmolality was calculat

170 Serum sodium was reduced (133.0 +/- 0.9 mmol/l furosemid

171 Serum sodium was significantly higher in the hypertonic

172 At higher doses, serum sodium was significantly increased; AVP antagonism

173 Because ascites is associated with low serum sodium, we evaluated serum sodium as an independen

174 d upon listing MELD with and without listing serum sodium were 0.883 and 0.897, respectively, and at

175 SDNN, creatinine, and serum sodium were related to progressive heart failure d

176 left ventricular end-systolic diameter, and serum sodium were significant predictors of all-cause mo

177 ests, pulmonary capillary wedge pressure and serum sodium were strong predictors of survival (p < 0.0

178 stration of tolvaptan maintains an increased serum sodium with an acceptable margin of safety.