ライフサイエンスコーパス: hyperkalemia

1 injury, perineal necrotizing fasciitis, and hyperkalemia.

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

3 tiation and dysfunction of the CD and causes hyperkalemia.

4 eart failure even in the setting of moderate hyperkalemia.

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

6 cardiographic findings consistent with acute hyperkalemia.

7 es, is prescribed routinely for treatment of hyperkalemia.

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

9 creases its effectiveness as a treatment for hyperkalemia.

10 resulting from renal potassium retention and hyperkalemia.

11 nt disease characterized by hypertension and hyperkalemia.

12 is may contribute to potassium retention and hyperkalemia.

13 the nephron, pathways of ammoniagenesis, and hyperkalemia.

14 the pathophysiology and management of severe hyperkalemia.

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

16 llow clinicians to successfully treat severe hyperkalemia.

17 o new approaches to the management of severe hyperkalemia.

18 the physiologic response to aldosterone with hyperkalemia.

19 cute tumor lysis syndrome resulting in fatal hyperkalemia.

20 ponses to intravascular volume depletion and hyperkalemia.

21 r eplerenone or spironolactone, Ly caused no hyperkalemia.

22 nt disease characterized by hypertension and hyperkalemia.

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

24 tors improve clinical outcomes but can cause hyperkalemia.

25 Mendelian disease featuring hypertension and hyperkalemia.

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

27 HAII), a syndrome featuring hypertension and hyperkalemia.

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

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

30 Mendelian disease featuring hypertension and hyperkalemia.

31 veloped hyperkalemia and 6% developed severe hyperkalemia.

32 as well as spironolactone's relationship to hyperkalemia.

33 t and plasma urea levels, hypernatremia, and 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 sium secretion are not sufficient to explain hyperkalemia.

46 ntified complication of trimethoprim-induced hyperkalemia.

47 D, raising the concern for severe exertional hyperkalemia.

48 tified significant independent predictors of hyperkalemia.

49 sin-aldosterone system increases the risk of hyperkalemia.

50 Incident hyperkalemia and severe hyperkalemia.

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

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

53 by neonatal life-threatening hypovolemia and hyperkalemia.

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

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

56 n for hormonally mediated acne but can cause hyperkalemia.

57 ower serum potassium levels in patients with hyperkalemia.

58 hly point in patients with mild and moderate hyperkalemia.

59 8], or 16.8 g [n = 30] twice daily [moderate hyperkalemia]).

60 were hypotension (17.6%), dizziness (16.8%), hyperkalemia (13.2%), and worsening kidney function (12.

61 eceived zilebesiran than placebo experienced hyperkalemia (18 [5.5%] vs 6 [1.8%]), hypotension (14 [4

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

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

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

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

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

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

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

69 The prevalence of hyperkalemia among healthy young women taking spironolac

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

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

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

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

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

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

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

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

78 Hyperkalemia and doubling of creatinine were more likely

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

80 Hyperkalemia and hypertension was observed in approximat

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

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

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

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

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

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

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

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

89 Incident hyperkalemia and severe hyperkalemia.

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

91 Hyperkalemia and worsening renal function were rare in R

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

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

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

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

96 ute kidney injury, bradycardia, hypotension, hyperkalemia, and hospital length of stay were similar b

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

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

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

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

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

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

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

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

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

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

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

108 strategies to deal with both hypokalemia and hyperkalemia are provided as well as guidance for the us

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

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

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

112 % to 1.8% (difference 0.7%, p < 0.001), with hyperkalemia associated with death reported in 2 (0.05%)

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

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

115 2% (difference 3.4%, p < 0.0001) and serious hyperkalemia (associated with death or hospitalization)

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

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

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

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

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

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

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

123 The incidence of hyperkalemia caused by mineralocorticoid receptor antago

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

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

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

127 During hyperkalemia, despite the shortening of the action poten

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 .5 mEq/L), normokalemia (3.5-5.0 mEq/L), and hyperkalemia (>5 mEq/L) were observed at the index admis

145 Hyperkalemia (>5.5 mmol/l) has also been associated with

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

147 (hazard ratio, 1.66 [95% CI, 1.10-2.22]) and hyperkalemia (hazard ratio, 3.36 [95% CI, 1.08-10.41]),

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

149 These mice displayed hypertension, hyperkalemia, hyperactive NCC, and other features fully

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

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

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

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

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

155 showed marked hypertension with significant hyperkalemia, hyperchloremia and low renin.

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

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

158 on, or discontinuation due to events such as hyperkalemia, hyponatremia, and reduction in kidney func

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

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

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

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

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

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

165 The rate of hyperkalemia in healthy young women taking spironolacton

166 The rate of hyperkalemia in healthy young women taking spironolacton

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

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

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

170 Hyperkalemia in patients with renal failure is frequentl

171 Hyperkalemia in PHA II patients with PHA II mutations ma

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

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

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

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

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

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

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

179 2%, equivalent to the 0.76% baseline rate of hyperkalemia in this population.

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

181 Dyskalemia (i.e., hypokalemia and hyperkalemia) in heart failure is common because of hear

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

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

184 Hyperkalemia increases the organization of ventricular f

185 Hyperkalemia increases the risk of death and limits the

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

187 Hyperkalemia-induced depolarization of the resting membr

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

189 Hyperkalemia is a common electrolyte abnormality that ma

190 Hyperkalemia is a potentially life-threatening condition

191 Hyperkalemia is a potentially life-threatening electroly

192 Hyperkalemia is common in patients with impaired kidney

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

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

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

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

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

198 Hyperkalemia is one of the few potentially lethal electr

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

200 Hyperkalemia is the most frequent electrolyte abnormalit

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

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

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

204 ere similar between treatment arms, although hyperkalemia leading to treatment discontinuation occurr

205 ne system inhibitor therapy in the advent of hyperkalemia likely contributes the observed risk.

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

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

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

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

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

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

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

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

214 monitoring for complications of CKD, such as hyperkalemia, metabolic acidosis, hyperphosphatemia, vit

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

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

217 1 [6%]), grade 3 fatigue (n=1 [6%]), grade 4 hyperkalemia (n=1 [6%]), and grade 2 acute kidney injury

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

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

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

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

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

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

224 on to potentially reversible causes, such as hyperkalemia or hypoxia.

225 f life-threatening conditions such as severe hyperkalemia or pulmonary edema) during severe AKI allow

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

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

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

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

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

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

232 = 74], or 12.6 g [n = 74] twice daily [mild hyperkalemia] or 8.4 g [n = 26], 12.6 g [n = 28], or 16.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 The incidence of hyperkalemia-related discontinuation of the trial regime

252 ween treatment arms, with a low incidence of hyperkalemia-related permanent treatment discontinuation

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

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

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

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

257 When these processes are disrupted, hyperkalemia results.

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

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

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

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

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

263 thrice-weekly hemodialysis with predialysis hyperkalemia (serum potassium was 5.5 mmol/l or more) we

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

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

266 Rates of worsening renal function, hyperkalemia, symptomatic hypotension, and angioedema di

267 The rates of worsening renal function, hyperkalemia, symptomatic hypotension, and angioedema di

268 were the rates of worsening renal function, hyperkalemia, symptomatic hypotension, and angioedema.

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

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

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

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

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

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

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

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

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

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

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

280 hospitalization with acute kidney injury or hyperkalemia using Cox regression.

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

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

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

284 Readmission associated with hyperkalemia was higher with aldosterone antagonist ther

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

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

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

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

289 EF and current or a history of RAASi-related hyperkalemia were screened and 1195 were enrolled in the

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

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

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

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

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

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

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

297 r characterized by arterial hypertension and hyperkalemia with metabolic acidosis.

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

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

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