ライフサイエンスコーパス: hyponatremia

1 l tolerated, with only one grade 4 toxicity (hyponatremia).

2 al at risk for the unexpected development of hyponatremia.

3 in patients with euvolemic and hypervolemic hyponatremia.

4 hat cerebral salt wasting is a rare cause of hyponatremia.

5 d in patients with euvolemic or hypervolemic hyponatremia.

6 AVP receptor antagonism in the treatment of hyponatremia.

7 ectrolyte-free water--might be of benefit in hyponatremia.

8 e complication of overly rapid correction of hyponatremia.

9 med to identify risk factors associated with hyponatremia.

10 rmone secretion (SIADH) is a common cause of hyponatremia.

11 Risk varied continuously with worsening hyponatremia.

12 ia with renal involvement, coagulopathy, and hyponatremia.

13 e central nervous system typical of clinical hyponatremia.

14 ners tend to develop conditions that lead to hyponatremia.

15 ting with concurrent grade 3 hypokalemia and hyponatremia.

16 ese rats had significant water retention and hyponatremia.

17 e 3 nonhematologic toxicity was asymptomatic hyponatremia.

18 atients are normonatremic and never manifest hyponatremia.

19 lydipsic schizophrenic patients with chronic hyponatremia.

20 der that can occur after rapid correction of hyponatremia.

21 d encephalopathy that is caused by untreated hyponatremia.

22 e risk for myelinolysis due to correction of hyponatremia.

23 ally evolve several days after correction of hyponatremia.

24 ic patients and may result in fewer cases of hyponatremia.

25 ntiate between depletional versus dilutional hyponatremia.

26 included hospitalization with hypokalemia or hyponatremia.

27 s LGI1 antibodies were associated with serum hyponatremia.

28 were alcoholics and 33 (92%) presented with hyponatremia.

29 hildren due to the risk of hospital-acquired hyponatremia.

30 to differentiate hypotonic from nonhypotonic hyponatremia.

31 rload edemas and high-vasopressin-associated hyponatremias.

32 wo patients in the hypotonic group developed hyponatremia, 1 in each group developed hypernatremia, 2

33 (27%), leukopenia (16%), fatigue (11%), and hyponatremia (10%).

34 died: normonatremic animals and animals with hyponatremia (105 mmol/L) of 3-d duration.

35 per liter or less); 0.6 percent had critical hyponatremia (120 mmol per liter or less).

36 rum sodium (>135 mEq/L) at OLT, whereas mild hyponatremia (125-134 mEq/L) was present in 615 (28.3%)

37 e thrombocytopenia (16%), fatigue (15%), and hyponatremia (13%).

38 ences were observed in the primary outcomes (hyponatremia 44% vs 67% (p=0.29); liver toxicity 6% vs 0

39 cases in patients receiving dabrafenib) and hyponatremia (8 and 6 cases, respectively) were also rep

40 0 mg/m2) and one anorexia, hypoglycemia, and hyponatremia (800 mg/m2).

41 prised fatigue (22%), hypertension (9%), and hyponatremia (9%).

42 Thirteen percent had hyponatremia (a serum sodium concentration of 135 mmol p

43 Last, AVP may contribute to hyponatremia, a powerful predictor of poor outcome in HF

44 ed hazard ratio, 3.06 [CI, 2.04 to 4.58]) or hyponatremia (adjusted hazard ratio, 1.68 [CI, 1.24 to 2

45 he risk for illness and death from untreated hyponatremia against the risk for myelinolysis due to co

46 paration of a late-stage intermediate of the hyponatremia agent, mozavaptan.

47 to a greater extent than in cells exposed to hyponatremia alone.

48 Nausea, emesis, fatigue, dehydration, and hyponatremia also were more frequent with vorinostat.

49 The incidence of CPM correlates with hyponatremia, although its overall incidence is low.

50 nts included in the study, 1,215 (11.2%) had hyponatremia and 277 (2.5%) had hypernatremia at admissi

51 an increased urine Na+ concentration despite hyponatremia and a decreased urine K+ concentration desp

52 monitoring important disease states such as hyponatremia and diabetes.

53 aintain cell volume, and that in response to hyponatremia and EtOH withdrawal their volume increases

54 ing toxicities (n = 1 for each) were grade 3 hyponatremia and herpes zoster reactivation and grade 4

55 Hyponatremia and hyperkalemia in infancy can represent a

56 The impact of hyponatremia and hypernatremia on 6-mo and 1-yr direct m

57 outcomes were mean sodium level at 24 hours, hyponatremia and hypernatremia, weight gain, hypertensio

58 Hyponatremia and increasing body temperature may be rela

59 r the treatment of chronic rather than acute hyponatremia and is more likely to occur with a rapid ra

60 of the clinically debilitating condition of hyponatremia and its associated syndromes.

61 t this stage, investigations commonly showed hyponatremia and MRI hippocampal high T2 signal; functio

62 patients without polydipsia and intermittent hyponatremia and normal subjects.

63 nown reasons, in schizophrenic patients with hyponatremia and polydipsia, thereby placing them at inc

64 Hyponatremia and the hepatorenal syndrome result from wa

65 arathon runners to estimate the incidence of hyponatremia and to identify the principal risk factors.

66 re postparacentesis circulatory dysfunction, hyponatremia, and mortality.

67 Ascites, hyponatremia, and other findings indicative of hemodynam

68 ism, colitis, diarrhoea, decreased appetite, hyponatremia, and pneumonitis (each in two [1%]) in thos

69 ia, hyperbilirubinemia, renal insufficiency, hyponatremia, and prothrombin time prolongation (all P <

70 ic reactions included hypotension, vomiting, hyponatremia, anemia, thrombocytopenia, and infection at

71 ients sustaining rapid correction of chronic hyponatremia are at risk of osmotic demyelination syndro

72 al agents currently used in the treatment of hyponatremia are limited by inconsistent response and ad

73 lele were 2.4-6.4 times as likely to exhibit hyponatremia as subjects without the minor allele (after

74 in the renal water retention and dilutional hyponatremia associated with chronic heart failure.

75 SALT-1 and SALT-2, and 85% continued to have hyponatremia at entry in SALTWATER.

76 Hyponatremia at hospital admission is a well-known risk

77 All patients had hyponatremia at randomization in SALT-1 and SALT-2, and

78 ting toxicity-grade 3 transient asymptomatic hyponatremia at the 1.0-mg/kg dose level.

79 dose-limiting toxicity was reported (grade 3 hyponatremia at the 20 mg dose), therefore the maximum t

80 We investigated the effect of hyponatremia at the time of OLT on mortality and morbidi

81 For acute or severely symptomatic hyponatremia, both guidelines adopted the approach of gi

82 for patients with head injury, alkalosis, or hyponatremia, but in large volumes may lead to metabolic

83 represent a new approach to the treatment of hyponatremia by blocking tubular reabsorption of water b

84 d hyponatremia (HAH) with community-acquired hyponatremia (CAH) in HF patients with respect to outcom

85 me expansion, excessive water retention with hyponatremia can occur in the absence of increases in aq

86 ent hyponatremia in previous studies, and 2) hyponatremia can significantly alter brain morphology on

87 Chronic hyponatremia (CH) was induced 3 d before the hypothalami

88 iew discusses the diagnosis and treatment of hyponatremia, comparing the two guidelines and highlight

89 e a difference; regardless of volume status, hyponatremia complicating intracranial disease should be

90 Hyponatremia developed in 21 percent, and there were sig

91 However, there are few data about hyponatremia developing during hospitalization in patien

92 ons for the few patients in whom symptomatic hyponatremia develops.

93 ebrospinal fluid white-cell counts or severe hyponatremia did.

94 xibility protects against the development of hyponatremia even in the face of water intake that can a

95 Hyponatremia frequently poses a therapeutic challenge in

96 eport a newborn with severe hyperkalemia and hyponatremia from autosomal recessive pseudohypoaldoster

97 en requiring IVFs are at risk for developing hyponatremia from numerous stimuli for arginine vasopres

98 n-small cell lung cancer) who presented with hyponatremia had inappropriately elevated levels of AVP.

99 The present study compares hospital-acquired hyponatremia (HAH) with community-acquired hyponatremia

100 Hyponatremia has emerged as an important cause of race-r

101 experience with AVP receptor antagonists for hyponatremia has shown that these agents augment free wa

102 Patients with polydipsia and intermittent hyponatremia have greater ventricle-brain ratios (VBRs)

103 xis), ascites and some of its complications (hyponatremia, hepatic hydrothorax), hepatorenal syndrome

104 factor even in patients without preexisting hyponatremia; however, isolated hypernatremia may be sol

105 Thiazide/amiloride-treated mice showed hyponatremia, hyperkalemia, hypercalcemia, metabolic aci

106 dosterone deficiency, signs of which include hyponatremia, hyperkalemia, hypovolemia, elevated plasma

107 Laboratory examination revealed hyponatremia, hyperpotassemia, hypoproteinemia, hypogamm

108 ributed to PS-341 included thrombocytopenia, hyponatremia, hypokalemia, fatigue, and malaise.

109 findings included diarrhea, hypoalbuminemia, hyponatremia, hypokalemia, hypocalcemia, and hypomagnese

110 f inducing severe hypokalemia in addition to hyponatremia, hypotension, and worsening renal function.

111 he condition of patients with mild or marked hyponatremia improved (P<0.001 for all comparisons).

112 n, remain under investigation for dilutional hyponatremia in ADHF.

113 eatures of myelinolysis by rapidly reversing hyponatremia in animals.

114 Most cases of hyponatremia in children are due to the syndrome of appr

115 Causes of hyponatremia in children include the syndrome of appropr

116 lts in a high incidence of hospital-acquired hyponatremia in children.

117 Hyponatremia in cirrhosis has prognostic value and novel

118 er of poor survival previously attributed to hyponatremia in heart failure.

119 Thus, hyponatremia in hospitalized patients with a diagnosis o

120 otic stimuli is a common cause of dilutional hyponatremia in neurological disorders.

121 Chronic symptomatic hyponatremia in postmenopausal women can be associated w

122 Chronic hyponatremia in postmenopausal women is a common clinica

123 in patients with polydipsia and intermittent hyponatremia in previous studies, and 2) hyponatremia ca

124 nts who have euvolemia and hypervolemia with hyponatremia in the short term (</=30 days), but their s

125 The occurrence of hyponatremia in these patients has been associated with

126 inappropriate antidiuretic hormone SIADH and hyponatremia in these patients.

127 ced ascorbic acid uptake, namely evidence of hyponatremia-induced oxidative stress.

128 The hyponatremia-induced shift in water from the extracellul

129 , we showed that rapid correction of chronic hyponatremia induces severe alterations in proteostasis

130 CF due to elevated sweat chloride, recurrent hyponatremia, infantile FTT and lung disease identified

131 Infection, hypotension, hyponatremia, insomnia or stress, and benzodiazepine use

132 Hyponatremia is a common and challenging disorder.

133 Hyponatremia is a common water balance disorder that oft

134 imal and human studies revealed that chronic hyponatremia is a previously unrecognized cause of osteo

135 In conclusion, hyponatremia is a significant independent predictor of 6

136 Hyponatremia is associated with inappropriately elevated

137 Hyponatremia is associated with lethal outcome in ALF.

138 Hyponatremia is associated with reduced survival in pati

139 The treatment for hyponatremia is chosen on the basis of duration and symp

140 Hyponatremia is common in patients with conditions such

141 Hyponatremia is frequently associated with neurological

142 Hypotonic hyponatremia is further differentiated on the basis of u

143 Although hyponatremia is known to be associated with osteoporosis

144 findings indicate that oxcarbazepine-induced hyponatremia is not attributable to the syndrome of inap

145 At present, therapy for acute and chronic hyponatremia is often ineffective and poorly tolerated.

146 ium deficiency, is the culprit in dilutional hyponatremia, isotonic saline administration may further

147 mEq/L) was present in 615 (28.3%) and severe hyponatremia (<125 mEq/L) in 65 (3.0%).

148 sopressors (18%), pulmonary edema (14%), and hyponatremia<130 mmol/L (14%).

149 Hyponatremia may worsen HE; it should be prevented as fa

150 Chronic symptomatic hyponatremia (mean [SD] sodium level 111 [12] mmol/L) wa

151 complications, specifically volume overload, hyponatremia, metabolic alkalosis, uremia, and hyperglyc

152 All 3 patients developed hyponatremia; none had faciobrachial dystonic seizures o

153 Hyponatremia occurs in a substantial fraction of nonelit

154 timulation of ENaC likely contributes to the hyponatremia of adrenal insufficiency.

155 s to be elevated in nearly all patients with hyponatremia of malignancy.

156 Treatment of hypotonic hyponatremia often challenges clinicians on many counts.

157 ver, data are sparse regarding the impact of hyponatremia on outcome following OLT.

158 ients, including four with fatigue, two with hyponatremia, one with muscle spasm, and one with atrial

159 oor outcomes than the rate of development of hyponatremia or the absolute decrease in the serum sodiu

160 y for mild attacks (mild pain, no paresis or hyponatremia) or until hemin is available.

161 d AHF patients may have renal insufficiency, hyponatremia, or an inadequate response to traditional d

162 Deaths result from hyperthermia, hyponatremia, or cerebral edema.

163 likely to have Child-Pugh class C cirrhosis, hyponatremia, or refractory ascites.

164 lar filtration rate <60 ml/min/1.73 m(2); 2) hyponatremia; or 3) diuretic resistance (urine output </

165 were highly correlated with the presence of hyponatremia (p < 0.00001).

166 C-reactive protein (CRP) (P = .0009); worse hyponatremia (P = .02); higher KSHV VL (P = .016), and h

167 l plasma ANP levels were not associated with hyponatremia (p = 0.73).

168 In total, 111 patients with hyponatremia received oral tolvaptan for a mean follow-u

169 fter discontinuation of tolvaptan on day 30, hyponatremia recurred.

170 rminal pro-B natriuretic peptide levels, and hyponatremia reflected greater neurohormonal activation.

171 Renal dysfunction, diuretic resistance, and hyponatremia represent treatment impediments.

172 Abrupt correction of hyponatremia resulted in vigorous activation of both the

173 e; this may help to attenuate the developing hyponatremia resulting from water loading when vasopress

174 he Study of Ascending Levels of Tolvaptan in Hyponatremia (SALT-1 and SALT-2).

175 alyzed, there were 1274 patients (0.8%) with hyponatremia (serum sodium <135 mmol/L), 162,829 (97.3%)

176 ted with serum sodium concentration and with hyponatremia (serum sodium concentration < or =135 mEq/L

177 Hyponatremia (serum sodium concentration, <135 mmol per

178 In patients with hyponatremia, serum sodium levels significantly increase

179 xperience suggest that correction of chronic hyponatremia should be kept at a rate less than 10 mmol/

180 Patients with severe hyponatremia tended to have a longer stay in the ICU (me

181 we present a practical approach to managing hyponatremia that centers on two elements: a diagnostic

182 rements is associated with increased risk of hyponatremia that results in morbidity and mortality in

183 d at the pathogenesis and putative causes of hyponatremia, the case-specific clinical and laboratory

184 Hyponatremia, the most frequent electrolyte disorder, is

185 rst-line treatment for most forms of chronic hyponatremia, therapy to increase renal free water excre

186 ize sodium from bone stores during prolonged hyponatremia, thereby leading to a resorptive osteoporos

187 ments for hypertension, but thiazide-induced hyponatremia (TIH), a clinically significant adverse eff

188 In patients with euvolemic or hypervolemic hyponatremia, tolvaptan, an oral vasopressin V2-receptor

189 metabolic characteristics of overhydration, hyponatremia, uremia, hyperglycemia, and alkalosis.

190 ocin is not receptor-selective and may cause hyponatremia via V2 receptor mediated antidiuresis.

191 ing for age, sex, region, and comorbidities, hyponatremia was a significant independent predictor of

192 inositol content in animals with uncorrected hyponatremia was about 50% of that found in normonatremi

193 The occurrence of hyponatremia was also decreased by albumin, compared wit

194 Hyponatremia was apparent in the isotonic crystalloid- a

195 Morbidity associated with hyponatremia was assessed, including length of hospitali

196 On univariate analyses, hyponatremia was associated with substantial weight gain

197 On multivariate analysis, hyponatremia was associated with weight gain (odds ratio

198 Hyponatremia was defined as a serum sodium concentration

199 One grade 4 event, asymptomatic hyponatremia, was judged to be unrelated to GDC-0449.

200 Both types of hyponatremia were associated with increased mortality, l

201 ic patients with polydipsia and intermittent hyponatremia were first assigned to either normal fluid

202 sweat chloride, infantile FTT, and recurrent hyponatremia were homozygous for a novel missense varian

203 ic patients with (n = 6) and without (n = 8) hyponatremia were identified based on past and current i

204 rmalization of serum sodium in patients with hyponatremia were observed in the tolvaptan group but no

205 history of tick bite, thrombocytopenia, and hyponatremia were often absent at initial presentation.

206 The effects of hyperammonemia and hyponatremia were synergistic.

207 c fluid associated with a lower incidence of hyponatremia when compared with hypotonic fluid for main

208 monstrated that hypotonic fluids cause acute hyponatremia, whereas 0.9% sodium chloride (NaCl) effect

209 ody-mass-index extremes were associated with hyponatremia, whereas female sex, composition of fluids

210 with oxcarbazepine showed the development of hyponatremia, which in most instances was asymptomatic.

211 opeptin concentrations from 50 patients with hyponatremia who underwent hypertonic saline infusion.

212 luid is associated with a lower incidence of hyponatremia, without evidence of an increase in adverse