ライフサイエンスコーパス: hyperkalemia

1 tiation and dysfunction of the CD and causes hyperkalemia.

2 eart failure even in the setting of moderate hyperkalemia.

3 sin-aldosterone system increases the risk of hyperkalemia.

4 (+/FHHt) mice, which could contribute to the hyperkalemia.

5 cardiographic findings consistent with acute hyperkalemia.

6 es, is prescribed routinely for treatment of hyperkalemia.

7 the organization and/or termination of VF by hyperkalemia.

8 creases its effectiveness as a treatment for hyperkalemia.

9 resulting from renal potassium retention and hyperkalemia.

10 nt disease characterized by hypertension and hyperkalemia.

11 is may contribute to potassium retention and hyperkalemia.

12 the nephron, pathways of ammoniagenesis, and hyperkalemia.

13 the pathophysiology and management of severe hyperkalemia.

14 id bioactivity in patients who have hypo- or hyperkalemia.

15 llow clinicians to successfully treat severe hyperkalemia.

16 o new approaches to the management of severe hyperkalemia.

17 the physiologic response to aldosterone with hyperkalemia.

18 cute tumor lysis syndrome resulting in fatal hyperkalemia.

19 ponses to intravascular volume depletion and hyperkalemia.

20 nt disease characterized by hypertension and hyperkalemia.

21 se subgroups, as was the incremental risk of hyperkalemia.

22 r eplerenone or spironolactone, Ly caused no hyperkalemia.

23 tors improve clinical outcomes but can cause hyperkalemia.

24 Mendelian disease featuring hypertension and hyperkalemia.

25 (PHA II), characterized by hypertension and hyperkalemia.

26 HAII), a syndrome featuring hypertension and hyperkalemia.

27 ting acid-base status, low urine output, and hyperkalemia.

28 , and many treated patients were at risk for hyperkalemia.

29 Mendelian disease featuring hypertension and hyperkalemia.

30 veloped hyperkalemia and 6% developed severe hyperkalemia.

31 as well as spironolactone's relationship to hyperkalemia.

32 t and plasma urea levels, hypernatremia, and hyperkalemia.

33 Incident hyperkalemia and severe hyperkalemia.

34 PHAII), a disease featuring hypertension and hyperkalemia.

35 endelian disease featuring hypertension with hyperkalemia.

36 disease with salt-sensitive hypertension and hyperkalemia.

37 at age 4 associated with rhabdomyolysis and hyperkalemia.

38 ension of PHAII but does not account for the hyperkalemia.

39 d a decreased urine K+ concentration despite hyperkalemia.

40 ed within 2 days after birth, most likely of hyperkalemia.

41 been beneficial compared with the results of hyperkalemia.

42 at room temperature, manifesting as apparent hyperkalemia.

43 duction in the amount of this isoform during hyperkalemia.

44 neys, renal insufficiency, hypertension, and hyperkalemia.

45 ntified complication of trimethoprim-induced hyperkalemia.

46 D, raising the concern for severe exertional hyperkalemia.

47 ies, block of particular channels, and hypo-/hyperkalemia.

48 e effects, however, such as hypertension and hyperkalemia.

49 by neonatal life-threatening hypovolemia and hyperkalemia.

50 out mice exhibited salt wasting, low BP, and hyperkalemia.

51 was associated with a 2-fold higher risk of hyperkalemia.

52 n for hormonally mediated acne but can cause hyperkalemia.

53 ower serum potassium levels in patients with hyperkalemia.

54 hly point in patients with mild and moderate hyperkalemia.

55 th placebo, a reduction in the recurrence of hyperkalemia.

56 sium secretion are not sufficient to explain hyperkalemia.

57 8], or 16.8 g [n = 30] twice daily [moderate hyperkalemia]).

58 atinine levels and a doubling of the rate of hyperkalemia (18.7%, vs. 9.1% in the placebo group) but

59 Dietary hypo- and hyperkalemia (2.8 +/- 0.1 and 6.8 +/- 0.3 mM) did not af

60 s 3.5%), hypotension (4.2% versus 2.1%), and hyperkalemia (2.8% versus 0.5%), respectively (all P<0.0

61 not different between groups at the time of hyperkalemia, 320+/-74 versus 298+/-49 for SPK and K(Tx)

62 Combination therapy increased the risk of hyperkalemia (6.3 events per 100 person-years, vs. 2.6 e

63 ia (14%), peripheral sensory neuropathy, and hyperkalemia (9% each).

64 a contributing factor to this case of fatal hyperkalemia after administration of succinylcholine, wi

65 The prevalence of hyperkalemia among healthy young women taking spironolac

66 laboratory values determined, 15% developed hyperkalemia and 6% developed severe hyperkalemia.

67 hat other mechanisms are responsible for the hyperkalemia and acidosis in this model.

68 onic kidney disease had higher rates of both hyperkalemia and acute kidney failure in the early (1.3%

69 ndary outcomes and adverse events, including hyperkalemia and acute kidney injury, were also similar

70 with reduced ejection fraction but can cause hyperkalemia and acute kidney injury.

71 nockout mice (Scnn1a(Pax8/LC1)) that exhibit hyperkalemia and body weight loss when kept on a regular

72 Safety end points included hyperkalemia and changes in renal function.

73 Among patients with hyperkalemia and diabetic kidney disease, patiromer star

74 Hyperkalemia and doubling of creatinine were more likely

75 e form of human hypertension associated with hyperkalemia and hyperchloremic metabolic acidosis.

76 Hyperkalemia and hypertension was observed in approximat

77 (PHAII) is an autosomal dominant disorder of hyperkalemia and hypertension.

78 We report a newborn with severe hyperkalemia and hyponatremia from autosomal recessive p

79 l insufficiency appears to increase risk for hyperkalemia and limits the use of the drug in patients

80 n, which features arterial hypertension with hyperkalemia and metabolic acidosis, unmasked a complex

81 AAs with HF exhibited less hyperkalemia and more hypokalemia with spironolactone co

82 We assessed hyperkalemia and outcomes in African Americans (AAs; n=1

83 ssium or creatinine concentrations, although hyperkalemia and renal dysfunction are common.

84 The risk of hyperkalemia and renal failure was higher in those with

85 Incident hyperkalemia and severe hyperkalemia.

86 In clinical practice, the incidence of hyperkalemia and worsening renal function and adequacy o

87 Hyperkalemia and worsening renal function were rare in R

88 anding of the pathophysiology that underlies hyperkalemia, and a rational approach to its management.

89 Safety outcomes included mortality, hyperkalemia, and acute kidney injury.

90 proteinuria, hyperbilirubinemia, back pain, hyperkalemia, and anorexia (n = 1 each).

91 but lower proportions with renal impairment, hyperkalemia, and cough than the enalapril group.

92 characterized by the triad of hyperuricemia, hyperkalemia, and hyperphosphatemia and is caused by the

93 aried from acute renal failure, proteinuria, hyperkalemia, and melena with minimal perturbation of ho

94 esistance to aldosterone, with salt wasting, hyperkalemia, and metabolic acidosis.

95 ism type II (PHA-II)--features hypertension, hyperkalemia, and metabolic acidosis.

96 n from cardiac arrest caused by hypovolemia, hyperkalemia, and primary arrhythmia.

97 al dominant disorder featuring hypertension, hyperkalemia, and renal tubular acidosis.

98 promote the desired physiologic response to hyperkalemia, and the fact that it is induced downstream

99 nal and novel ways to approach management of hyperkalemia; and discusses the need for further researc

100 in: diabetes mellitus, hypercholesterolemia, hyperkalemia, anemia, and elevated angiotensin II.

101 ognition and expeditious treatment of severe hyperkalemia are expected to save lives.

102 ies supporting the usefulness of the TTKG in hyperkalemia are limited to case series.

103 II are curious genetic disorders that share hyperkalemia as a predominant finding.

104 fined as any [K] > or = 5.5 mEq/l and severe hyperkalemia as any [K] > or = 6.0.

105 s, have sparked interest in the treatment of hyperkalemia, as well as the potential use of renin-angi

106 % to 1.8% (difference 0.7%, p < 0.001), with hyperkalemia associated with death reported in 2 (0.05%)

107 We assessed the incidence and predictors of hyperkalemia associated with dose reduction, study drug

108 To determine whether the risk of hyperkalemia associated with use of MRAs for patients wi

109 2% (difference 3.4%, p < 0.0001) and serious hyperkalemia (associated with death or hospitalization)

110 Although the extremes of hypokalemia and hyperkalemia at 4 weeks were associated with increased r

111 mponents of the primary outcome and rates of hyperkalemia at 6 months.

112 We further conclude that hyperkalemia becomes the determining factor in regulatin

113 e to exhaust other alternatives for managing hyperkalemia before turning to these largely unproven an

114 of morbidity and mortality in patients with hyperkalemia but these associations appear disconnected

115 lon, was approved in 1958 as a treatment for hyperkalemia by the US Food and Drug Administration, 4 y

116 The traditional views that hyperkalemia can be reliably diagnosed by electrocardiog

117 The incidence of hyperkalemia caused by mineralocorticoid receptor antago

118 isplayed thiazide-treatable hypertension and hyperkalemia, concurrent with NCC hyperphosphorylation.

119 ctrocardiogram and that particular levels of hyperkalemia confer cardiotoxic risk have been challenge

120 Four independent baseline predictors of hyperkalemia (defined as > or =6.0 mEq/L) were identifie

121 During hyperkalemia, despite the shortening of the action poten

122 Hyperkalemia developed in 48 of 138 (35%) patients with

123 a suggest that the clinical context in which hyperkalemia develops is at least as important as the de

124 nherited syndrome featuring hypertension and hyperkalemia due to increased renal NaCl reabsorption an

125 HAII), a disease featuring hypertension with hyperkalemia, due to altered activity of specific Na-Cl

126 be monitored closely for the development of hyperkalemia, especially if they have concurrent renal i

127 y disease (CKD), but their use is limited by hyperkalemia, especially when associated with RAS inhibi

128 disease, which further heightens the risk of hyperkalemia, especially when renin-angiotensin-aldoster

129 n MRA at baseline and the risk of subsequent hyperkalemia for those newly treated with an MRA during

130 Candesartan increased the rate of aggregate hyperkalemia from 1.8% to 5.2% (difference 3.4%, p < 0.0

131 and died between 24 and 36 h, probably from hyperkalemia (gammaENaC -/- 18.3 mEq/l, control litterma

132 e rare familial syndrome of hypertension and hyperkalemia (Gordon syndrome, or pseudohypoaldosteronis

133 ovolemia group, 29 mm (95% CI, 26-32) in the hyperkalemia group, and 25 mm (95% CI, 22-28) in the pri

134 serum potassium level into mild or moderate hyperkalemia groups and received 1 of 3 randomized start

135 Hyperkalemia >5.5 mmol/l(-1) occurred in 3% and 0.2% of

136 e in potassium levels or in the incidence of hyperkalemia (> or =5.5 meq/L) on DRSP/E2 compared with

137 proves outcomes without an excess of risk of hyperkalemia (> or =6.0 mEq/L) when periodic monitoring

138 .5 mEq/L), normokalemia (3.5-5.0 mEq/L), and hyperkalemia (>5 mEq/L) were observed at the index admis

139 emoving potassium from the body and treating hyperkalemia have been tested in clinical trials.

140 induce worsening of renal function (WRF) and hyperkalemia (HK).

141 atures of pseudohypoaldosteronism, including hyperkalemia, hyperaldosteronism, and metabolic acidosis

142 ombination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine tox

143 /amiloride-treated mice showed hyponatremia, hyperkalemia, hypercalcemia, metabolic acidosis, and inc

144 sion and renal tubule dysfunction, including hyperkalemia, hypercalciuria and acidosis, often complic

145 Wnk4(PHAII) mice have higher blood pressure, hyperkalemia, hypercalciuria and marked hyperplasia of t

146 a Mendelian disease featuring hypertension, hyperkalemia, hyperchloremia, and metabolic acidosis.

147 Risks of routine prophylaxis include hyperkalemia, hypoglycemia, photosensitivity, thrombocyt

148 The rates of hyperkalemia, hypotension, and renal impairment/renal fa

149 ciency, signs of which include hyponatremia, hyperkalemia, hypovolemia, elevated plasma renin activit

150 We looked at the incidence of hyperkalemia in 34 type I diabetic SPK recipients transp

151 We analyzed rates of hyperkalemia in 974 healthy young women taking spironola

152 We explored the incidence and predictors of hyperkalemia in a broad population of heart failure pati

153 apical ENaC localization, and caused severe hyperkalemia in AS(-/-) mice.

154 The rate of hyperkalemia in healthy young women taking spironolacton

155 The rate of hyperkalemia in healthy young women taking spironolacton

156 idemiology, pathophysiology, and outcomes of hyperkalemia in heart failure; provides an overview of t

157 s a salt-sensitive form of hypertension with hyperkalemia in humans caused by mutations in the with-n

158 Hyponatremia and hyperkalemia in infancy can represent a variety of renal

159 Hyperkalemia in patients with renal failure is frequentl

160 Hyperkalemia in PHA II patients with PHA II mutations ma

161 al K(+) channel ROMK, likely contributing to hyperkalemia in PHAII.

162 igh K intake was diminished with significant hyperkalemia in Romk1(-/-) mice.

163 but can cause reversible nephrotoxicity and hyperkalemia in the newborn.

164 ontributed to the aldosterone resistance and hyperkalemia in these mice.

165 rease in dietary potassium would not provoke hyperkalemia in this population despite treatment with e

166 r acne is equivalent to the baseline rate of hyperkalemia in this population.

167 to obtain a profile for the baseline rate of hyperkalemia in this population.

168 2%, equivalent to the 0.76% baseline rate of hyperkalemia in this population.

169 children with Duchenne's muscular dystrophy: hyperkalemia in younger children and myocardial depressi

170 l monitoring and aggressive intervention for hyperkalemia, including hemodialysis if necessary, allow

171 pendent of treatment assignment, the risk of hyperkalemia increased with age > or =75 years, male gen

172 Hyperkalemia increases the organization of ventricular f

173 Hyperkalemia increases the risk of death and limits the

174 The CDTsc1KO mice provide a novel model for hyperkalemia induced exclusively by dysfunction of the C

175 Hyperkalemia-induced depolarization of the resting membr

176 simulated hyperkalemia prevented all of the hyperkalemia-induced VF changes.

177 Hyperkalemia is a common electrolyte abnormality that ma

178 Hyperkalemia is a potentially life-threatening condition

179 Hyperkalemia is a potentially life-threatening electroly

180 Hyperkalemia is common in patients with impaired kidney

181 ps is at least as important as the degree of hyperkalemia is in determining patient outcome.

182 The risk of hyperkalemia is increased in symptomatic heart failure p

183 ated patients with symptomatic HFrEF, severe hyperkalemia is more likely during treatment with enalap

184 ve intervention for tumor lysis syndrome and hyperkalemia is necessary for safe drug administration.

185 ole of mTOR in renal potassium excretion and hyperkalemia is not known.

186 Hyperkalemia is one of the few potentially lethal electr

187 These findings suggest that hyperkalemia is the critical event following Chironex fl

188 Hyperkalemia is the most frequent electrolyte abnormalit

189 rm of renal tubular acidosis associated with hyperkalemia is usually attributable to real or apparent

190 s had a 36% incidence of transient perinatal hyperkalemia (K+>7.0 meq/L) and a mild reversible renal

191 ures (potassium >5.5, >6.0, and <3.5 mmol/l; hyperkalemia leading to study-drug discontinuation or ho

192 by further decreasing the already reduced-by-hyperkalemia local excitability, causing extended conduc

193 pproaches to the prevention and treatment of hyperkalemia may be on the horizon.

194 Regulation of Kv4 channel inactivation by hyperkalemia may help to explain the pathophysiology of

195 dysfunction; however, the perceived risk of hyperkalemia may limit implementation of this therapeuti

196 Acute treatment for hyperkalemia may not be tolerated in the long term.

197 ildren with Duchenne's muscular dystrophy as hyperkalemia may occur in young males and myocardial dep

198 The increased incidence of hyperkalemia may, in part, be secondary to decreased sod

199 We hypothesized that hyperkalemia-mediated depolarization of the reversal pot

200 ccepted indications include volume overload, hyperkalemia, metabolic acidosis, overt uremia, and even

201 ne of the following criteria was met: severe hyperkalemia, metabolic acidosis, pulmonary edema, blood

202 1 [6%]), grade 3 fatigue (n=1 [6%]), grade 4 hyperkalemia (n=1 [6%]), and grade 2 acute kidney injury

203 e adjusted hazard ratios for hypokalemia and hyperkalemia, normokalemia as reference, were 2.35 (95%

204 , Rictorfl/fl Ksp-Cre mice rapidly developed hyperkalemia on a high-K+ diet, despite a 10-fold increa

205 Among outpatients with hyperkalemia, open-label sodium zirconium cyclosilicate

206 No significant differences in hyperkalemia or anemia were found between the two groups

207 sium >6.0 mmol/l, and of hospitalization for hyperkalemia or discontinuation of study medication due

208 ed or depolarized by various factors such as hyperkalemia or hypokalemia in the long term, or by dela

209 y of eplerenone in patients at high risk for hyperkalemia or worsening renal function (WRF) in EMPHAS

210 sis of subgroups of patients at high risk of hyperkalemia or WRF (patients >/= 75 years of age, with

211 s with HF-REF may be due to fear of inducing hyperkalemia or WRF in high-risk patients.

212 even in subgroups at high risk of developing hyperkalemia or WRF.

213 n from cardiac arrest caused by hypovolemia, hyperkalemia, or primary arrhythmia (i.e., ventricular f

214 cardiac arrest caused by either hypovolemia, hyperkalemia, or primary arrhythmia.

215 = 74], or 12.6 g [n = 74] twice daily [mild hyperkalemia] or 8.4 g [n = 26], 12.6 g [n = 28], or 16.

216 o were receiving RAAS inhibitors and who had hyperkalemia, patiromer treatment was associated with a

217 mol/L developed in 62.5% of patients; severe hyperkalemia (peak serum potassium concentration > or =

218 levels and ammonia production dictates that hyperkalemia per se can lead to acidosis.

219 We assessed incidence and predictors of hyperkalemia (potassium >/=5.5 mmol/L) and hypokalemia (

220 eatinine levels is mandated to avoid serious hyperkalemia (potassium concentration >5.5 mEq/L) and it

221 The incidence of hyperkalemia (potassium level >5.5 mEq/L) and severe hyp

222 emia (potassium level >5.5 mEq/L) and severe hyperkalemia (potassium level >6.0 mEq/L) among patients

223 an with patiromer (P<0.001); a recurrence of hyperkalemia (potassium level, >/=5.5 mmol per liter) oc

224 versus 5.8%; P=0.04) and had higher rates of hyperkalemia (potassium>5.5 mmol/L; 9.7% versus 4.2%; P<

225 FR had similar strengths of association with hyperkalemia/potassium level and with metabolic acidosis

226 ant increase in the risk of readmission with hyperkalemia, predominantly within 30 days after dischar

227 (K1) to normokalemic values during simulated hyperkalemia prevented all of the hyperkalemia-induced V

228 KWNK4, encoding WNK4, cause hypertension and hyperkalemia (pseudohypoaldosteronism type II, PHAII) by

229 etting of intravascular volume depletion and hyperkalemia, raising the question of how the kidney max

230 receiving spironolactone therapy, yielding a hyperkalemia rate of 0.72%, equivalent to the 0.76% base

231 nd heart failure readmission at 3 years, and hyperkalemia readmission at 30 days and 1 year.

232 at 3 years; and 2.9% vs 1.2% (P < .001) for hyperkalemia readmission within 30 days and 8.9% vs 6.3%

233 During VF, hyperkalemia reduced the maximum DF of the left ventricl

234 ng MRAs during the PARADIGM-HF trial, severe hyperkalemia remained more common in those randomly assi

235 nts with advanced age, male gender, baseline hyperkalemia, renal failure, diabetes, or combined RAAS

236 l K+ secretion in response to hypovolemia or hyperkalemia, respectively.

237 endelian syndrome featuring hypertension and hyperkalemia resulting from constitutive renal salt reab

238 When these processes are disrupted, hyperkalemia results.

239 drainage may be particularly susceptible to hyperkalemia secondary to sodium loss from the bladder-d

240 zirconium cyclosilicate in outpatients with hyperkalemia (serum potassium >/=5.1 mEq/L) recruited fr

241 tor blockers (ARBs) may increase the risk of hyperkalemia (serum potassium concentration >5 mmol/L) i

242 The proportion of patients with hyperkalemia (serum potassium level, >/=6 mmol per liter

243 Hyperkalemia (serum potassium level, >5.0 mmol per liter

244 vents were patient-reported hypoglycemia and hyperkalemia (serum potassium>5.5 mEq/L), respectively.

245 oup (P < .001 for all changes vs baseline by hyperkalemia starting-dose groups within strata).

246 ssion levels in humans causes a hypertension-hyperkalemia syndrome by altering renal Na(+) and K(+) t

247 mutations cause a familial hypertension and hyperkalemia syndrome known as pseudohypoaldosteronism t

248 pients appear to have a greater incidence of hyperkalemia than kidney alone transplant recipients.

249 ypotension, worsening of renal function, and hyperkalemia than was angiotensin-converting enzyme inhi

250 of mild, salt-sensitive hypertension without hyperkalemia that is characterized by upregulation of NC

251 ng cardiac disturbances such as ischemia and hyperkalemia, the extracellular potassium ion concentrat

252 dary endpoints included acute renal failure, hyperkalemia, the prevalence of hypotension, length of h

253 In those with moderate hyperkalemia, the reduction was 0.87 (95% CI, 0.60-1.14)

254 ial nephritis, hypertension and tendency for hyperkalemia, though none had rapid deterioration of ren

255 predispose certain patients presenting with hyperkalemia to a lower or higher threshold for toxicity

256 rial, we randomly assigned 753 patients with hyperkalemia to receive either ZS-9 (at a dose of 1.25 g

257 f first dose titration in patients with mild hyperkalemia was 0.35 (95% CI, 0.22-0.48) mEq/L for the

258 The rate of serious hyperkalemia was 5.5 percent in the eplerenone group and

259 The incidence of hyperkalemia was 73.5% in recipients of an SPK, while it

260 Readmission associated with hyperkalemia was higher with aldosterone antagonist ther

261 The incidence of serious hyperkalemia was minimal in both groups of patients.

262 similar between treatment groups, but severe hyperkalemia was more common in patients randomly assign

263 potension, progressive renal dysfunction, or hyperkalemia were documented in 60 patients (23%); other

264 CsA levels at the time of hyperkalemia were not different from those at the time o

265 ing an MRA at baseline, the overall rates of hyperkalemia were similar between treatment groups, but

266 neprilysin inhibition attenuates the risk of hyperkalemia when MRAs are combined with other inhibitor

267 indicate an inappropriate renal response to hyperkalemia, whereas values >2 during hypokalemia point

268 ein intake may lead to hyperphosphatemia and hyperkalemia, which are also mortality risk factors.

269 in patients with heart failure but can cause hyperkalemia, which contributes to reduced use of these

270 One factor may be the depolarizing nature of hyperkalemia, which results in continuing transmembrane

271 Patients with hyperkalemia who received ZS-9, as compared with those w

272 review summarizes the clinical data linking hyperkalemia with poor outcomes and discusses how the ef

273 age due to catatonic immobility led to acute hyperkalemia with the administration of succinylcholine.

274 oped renal dysfunction, of whom 25 developed hyperkalemia within three months.