ライフサイエンスコーパス: hypokalemia

1 tion, or--less frequently--hypertension with hypokalemia.

2 ium deficiency is frequently associated with hypokalemia.

3 y alone, however, does not necessarily cause hypokalemia.

4 truction, complicated by severe diarrhea and hypokalemia.

5 irst course of therapy, and in patients with hypokalemia.

6 tassium gradient was high in the presence of hypokalemia.

7 duct mediates K+ conservation during chronic hypokalemia.

8 ity characterized by hypophosphatemia and/or hypokalemia.

9 fter presenting with metabolic alkalosis and hypokalemia.

10 easing K+ transport from blood to CSF during hypokalemia.

11 is activated by low potassium intake and by hypokalemia.

12 ther away from the INa threshold, such as in hypokalemia.

13 E has an important role in the prevention of hypokalemia.

14 , vs. 9.1% in the placebo group) but reduced hypokalemia.

15 e of electrolyte abnormalities, particularly hypokalemia.

16 pplied to monitor patients at risk for hyper/hypokalemia.

17 er blood volume and pressure without causing hypokalemia.

18 atch-clamped ventricular myocytes exposed to hypokalemia (1.0-3.5 mmol/L) in the absence or presence

19 reported adverse events were pyrexia (18%), hypokalemia (15%), and hypophosphatemia (15%).

20 re anemia (36%), thrombocytopenia (21%), and hypokalemia (17%).

21 brile neutropenia (47% v 35%, respectively), hypokalemia (18% v 11%, respectively), thrombocytopenia

22 In intact hearts, moderate hypokalemia (2.7 mmol/L) significantly increased tissue

23 verload with BayK8644, and ionic stress with hypokalemia; 2), computer simulations using a physiologi

24 22% in arms A, B, and C, respectively), and hypokalemia (21%, 15%, and 5% in arms A, B, and C, respe

25 a (5.0% v 14.4%), stomatitis (1.3% v 13.6%), hypokalemia (3.6% v 10.8%), and treatment-related deaths

26 itis, palmar-plantar erythrodysesthesia, and hypokalemia (400 mg twice per day; n = 1); and grade 3 t

27 5%), elevated conjugated bilirubin (5%), and hypokalemia (5%).

28 In children with leukemia, grade 4 hypokalemia (50 mg/m(2)), grade 3 diarrhea (85 mg/m(2)),

29 Hypokalemia (6 cases in patients receiving vemurafenib a

30 or 2; the most frequent grade >/= 3 AEs were hypokalemia (8.9%), thrombocytopenia (8.0%), and fatigue

31 opic drugs are administered to patients with hypokalemia, abnormal T wave morphology, HCV infection,

32 stinal peptideoma [VIPoma], watery diarrhea, hypokalemia-achlorhydria [WDHA], glucagonoma [glucagonom

33 one were more likely to be hospitalized with hypokalemia (adjusted hazard ratio, 3.06 [CI, 2.04 to 4.

34 Hypokalemia also leads to worse outcomes in patients wit

35 imbalances, such as reduced serum K+ levels (hypokalemia), also trigger these potentially fatal arrhy

36 y, one must consider CF when confronted with hypokalemia and alkalosis in a previously healthy patien

37 sade de pointes often occurs with underlying hypokalemia and bradycardia.

38 mg/m2, including nausea, vomiting, diarrhea, hypokalemia and cardiovascular problems.

39 K current suppression by hypokalemia and dofetilide alone in the absence of CaMKI

40 riables associated with risk of TdP included hypokalemia and female gender; by contrast, persistent a

41 Although the extremes of hypokalemia and hyperkalemia at 4 weeks were associated

42 Likewise, the adjusted hazard ratios for hypokalemia and hyperkalemia, normokalemia as reference,

43 des of treatment failures, and incidences of hypokalemia and hypoglycemia.

44 iarrhea and vomiting with concurrent grade 3 hypokalemia and hyponatremia.

45 e of spironolactone was associated with less hypokalemia and improved survival in patients with sever

46 rption in outer medullary collecting duct in hypokalemia and in acid-base regulation in conditions th

47 on-dose-limiting grade 3 toxicities included hypokalemia and lymphopenia.

48 Concomitant magnesium deficiency aggravates hypokalemia and renders it refractory to treatment by po

49 ides a mechanism to explain the link between hypokalemia and torsade de pointes.

50 Long-term toxicities occurred in 2 patients: hypokalemia and tremor, both grade III, on days 370 and

51 ut (Nedd4L(Pax8/LC1) ) mice exhibited severe hypokalemia and urinary K(+) wasting.

52 genetic condition characterized by polyuria, hypokalemia, and alkalosis.

53 e, night sweats, diarrhea, nausea, vomiting, hypokalemia, and cough.

54 mice demonstrated severe metabolic acidosis, hypokalemia, and early nephrocalcinosis.

55 rticoid receptors, causing sodium retention, hypokalemia, and hypertension.

56 ell as nephrotoxicity with secondary anemia, hypokalemia, and hypomagnesemia.

57 ing duct of mouse kidney caused hypotension, hypokalemia, and metabolic alkalosis, an exact mirror im

58 pe, characterized by renal salt loss, marked hypokalemia, and metabolic alkalosis.

59 of NaCl, K+, and water, causing hypovolemia, hypokalemia, and polyuria.

60 A combination of bradycardic stimulation, hypokalemia, and quinidine resulted in early afterdepola

61 of abnormal liver function tests, diarrhea, hypokalemia, and thrombocytopenia.

62 characterized by acute attacks of weakness, hypokalemia, and thyrotoxicosis of various etiologies.

63 ding KD diet to rats resulted in significant hypokalemia at 14 d but not at 6 d.

64 -limiting neutropenia, thrombocytopenia, and hypokalemia at 300 mg/m(2)/d.

65 everity was associated with injury severity, hypokalemia, baseline CIWA-Ar score, and established alc

66 respectively), rash, fatigue, anorexia, and hypokalemia, but not more late toxicity.

67 d endocytic degradation under low potassium (hypokalemia) conditions.

68 Hypokalemia developed in 5/51 (10%) and 6/56 patients (1

69 on is more effective in normokalemia than in hypokalemia due to the difference in dynamical threshold

70 isodic flaccid paralysis of muscle and acute hypokalemia during attacks.

71 nism in which NEDD4-2 deficiency exacerbates hypokalemia during dietary K(+) restriction primarily th

72 ill within the normal range and before frank hypokalemia ensues, in addition to the classic feedback

73 is dynamical threshold becomes much lower in hypokalemia, especially with respect to calcium, as pred

74 They found that hypokalemia evoked HERG channel ubiquitination, enhanced

75 nism, limitation of diuretics, correction of hypokalemia, exercise, and diet.

76 341 included thrombocytopenia, hyponatremia, hypokalemia, fatigue, and malaise.

77 mer were more likely to be hospitalized with hypokalemia for all 6 comparisons in which a statistical

78 de a strong diuretic regimen without causing hypokalemia for patients with fluid overload, including

79 Hypertension (grade 3, 12%) and hypokalemia (grade 3, 6%; grade 4, 3%) were the most fre

80 After adjustment for hypokalemia, HCV infection, HIV infection, and abnormal

81 g QT had significantly higher frequencies of hypokalemia, hepatitis C virus (HCV) infection, HIV infe

82 Patients with hypokalemia, hypermagnesemia, or postcardiac surgery atr

83 ded diarrhea, hypoalbuminemia, hyponatremia, hypokalemia, hypocalcemia, and hypomagnesemia; 14 patien

84 gation were female sex, QT-prolonging drugs, hypokalemia, hypocalcemia, hyperglycemia, high creatinin

85 f infusion-related reactions, renal failure, hypokalemia, hypomagnesemia, and anemia than patients in

86 and female survivors are fertile but exhibit hypokalemia, hypotonic polyuria, and apparent mineraloco

87 a resolution, at the risk of inducing severe hypokalemia in addition to hyponatremia, hypotension, an

88 annel aquaporin 2, and improved polyuria and hypokalemia in mutant mice.

89 nd K(+) balance and promotes hypotension and hypokalemia in response to Na(+) and K(+) depletion, res

90 /pendrin system may explain thiazide-induced hypokalemia in some patients.

91 d by various factors such as hyperkalemia or hypokalemia in the long term, or by delayed afterdepolar

92 oms or syndromes, including hypertension and hypokalemia (in patients with aldosteronoma), Cushing sy

93 tifying unbridled turnover as a mechanism of hypokalemia-induced arrhythmia.

94 n diuretics are used; and (3) concerns about hypokalemia-induced arrhythmias have been overstated.

95 differential diagnosis of corticosteroid or hypokalemia-induced myopathy in Crohn's disease.

96 notably including AQP2, is an early event in hypokalemia-induced NDI.

97 tion of Kir2.6 predisposes the sarcolemma to hypokalemia-induced paradoxical depolarization during at

98 inactive analogue KN-92, abolished EADs and hypokalemia-induced ventricular tachycardia/fibrillation

99 Chronic hypokalemia is known to induce renal structural and func

100 Hypokalemia is known to promote ventricular arrhythmias,

101 Hypokalemia is not addressed here.

102 =6.0 mEq/L, and a 4.7% absolute decrease in hypokalemia (K(+) <3.5 mEq/L).

103 Hypokalemia (low serum potassium level) is a common elec

104 LDO/salt + furosemide and was accompanied by hypokalemia (<3.4 mmol/l) that were rescued by spironola

105 t common gastrointestinal adverse event, and hypokalemia (<3.5 mEq/L) occurred in 5.6% of patients.

106 Hypokalemia (<3.5 mEq/L), normokalemia (3.5-5.0 mEq/L),

107 However, these hypokalemia-mediated changes occur in a handful of condi

108 ive haemorrhage in basal ganglia and chronic hypokalemia-mediated nephrocalcinosis and renal cysts.

109 ntal retardation, and electrolyte imbalance (hypokalemia, metabolic alkalosis, and hypomagnesemia).

110 autoimmune thrombocytopenia (n = 1; 2%), and hypokalemia (n = 1; 2%), which resolved spontaneously or

111 entified: heart failure (n=8), angina (n=2), hypokalemia (n=1), adverse antiarrhythmic drug treatment

112 ypercalcemia at 15 mg/m(2); hypophosphatemia/hypokalemia, neutropenia, and somnolence at 40 mg/m(2);

113 Transient elevation of liver enzymes and hypokalemia occurred frequently.

114 mmon adverse event (in 11% of the patients); hypokalemia occurred in 3%.

115 afety outcomes included hospitalization with hypokalemia or hyponatremia.

116 f SLC26A7 in states that are associated with hypokalemia or increased medullary tonicity.

117 rate or blood pressure, nor did it result in hypokalemia or worsening renal function.

118 ributing factors, such as drugs that promote hypokalemia; or using an alternative therapy.

119 e that Na-K pump inhibition by even moderate hypokalemia plays a critical role in promoting EAD-media

120 se to hyperkalemia, whereas values >2 during hypokalemia point to renal loss.

121 f hyperkalemia (potassium >/=5.5 mmol/L) and hypokalemia (potassium <3.5 mmol/L) and the relationship

122 tted to the study on the basis of documented hypokalemia (potassium of < 3.5 mmol/L) within the 24-hr

123 us 4.2%; P<0.046), as well as lower rates of hypokalemia (potassium<3.5 mmol/L; 5.6% versus 17.9%; P<

124 h severe hypoglycemia; 2) with limitation of hypokalemia, potassium supplementation could limit hypog

125 This observation provides insight into why hypokalemia promotes calcium-mediated triggered activity

126 thy, tremor, constipation, dyspnea, hypoxia, hypokalemia, rash, and edema.

127 Hypokalemia seen with heat stress is secondary to sweat

128 id-suppressible hyperaldosteronism may cause hypokalemia, suppressed plasma renin activity, and hyper

129 served that the stimulus needed was lower in hypokalemia than in normokalemia in both computer simula

130 ver, the mechanism of renal K(+) wasting and hypokalemia that develop in individuals with ROMK Bartte

131 ctors were simultaneously present, including hypokalemia that was the most common (52%).

132 e of the patients reported CTC grades 3 to 4 hypokalemia, three reported CTC grade 3 acute renal inju

133 exposed to either oxidative stress (H2O2) or hypokalemia to induce bradycardia-dependent EADs at a lo

134 A patient with hypertension and hypokalemia underwent an adrenal venous effluent samplin

135 placebo group (P=0.002), whereas the rate of hypokalemia was 8.4 percent in the eplerenone group and

136 um tremens (odds ratio, 6.08; p = 0.01), and hypokalemia was borderline significant (odds ratio, 3.23

137 doubling of creatinine were more likely and hypokalemia was less likely in patients receiving spiron

138 Hypokalemia was resolved in all patients (2.6 mmol/L +/-

139 Hypokalemia was seen in 12 children (48%) receiving the

140 s assigned to 32 degrees C, the incidence of hypokalemia was similar in both groups.

141 orticoid-related toxicities (hypertension or hypokalemia) was reduced by adding low-dose prednisone.

142 Hypomagnesemia, hypocalcemia, and hypokalemia were not found.

143 ytopenia, abnormal liver function tests, and hypokalemia were reported more often for SRL-ST therapy.

144 including fluid retention, hypertension, and hypokalemia, were more frequently reported in the abirat

145 Hypokalemia, which causes only intracellular acidosis, c

146 Hypokalemia, which frequently occurs among dialysis pati

147 nal failure, and metabolic alkalosis without hypokalemia, which were all corrected with salt replacem

148 the kidney, but is most likely secondary to hypokalemia with ECF volume contraction.

149 elman-like syndrome (fortuitous discovery of hypokalemia with hypomagnesemia and/or hypocalciuria in

150 lt to control the patient's hypertension and hypokalemia with medical therapy alone.

151 with HF exhibited less hyperkalemia and more hypokalemia with spironolactone compared with non-AAs an

152 ter modeling revealed that EAD generation by hypokalemia (with or without dofetilide) required Na-K p