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1 laboratory monitoring AEs (hyperkalemia and hypokalemia).
2 er blood volume and pressure without causing hypokalemia.
3 tion, or--less frequently--hypertension with hypokalemia.
4 ium deficiency is frequently associated with hypokalemia.
5 y alone, however, does not necessarily cause hypokalemia.
6 truction, complicated by severe diarrhea and hypokalemia.
7 irst course of therapy, and in patients with hypokalemia.
8 tassium gradient was high in the presence of hypokalemia.
9 duct mediates K+ conservation during chronic hypokalemia.
10 ity characterized by hypophosphatemia and/or hypokalemia.
11 fter presenting with metabolic alkalosis and hypokalemia.
12 easing K+ transport from blood to CSF during hypokalemia.
13 ut was associated with an increased risk for hypokalemia.
14 ing, fatigue, hypersensitivity reaction, and hypokalemia.
15 d risk of hyperkalemia and a reduced risk of hypokalemia.
16 resis as well as renal potassium wasting and hypokalemia.
17 locorticoid receptor, which is enhanced with hypokalemia.
18 erum potassium levels and a low incidence of hypokalemia.
19 od was applied to predict the development of hypokalemia.
20 tical role in human ectopic heartbeats under hypokalemia.
21 is activated by low potassium intake and by hypokalemia.
22 E has an important role in the prevention of hypokalemia.
23 pplied to monitor patients at risk for hyper/hypokalemia.
24 ther away from the INa threshold, such as in hypokalemia.
25 , vs. 9.1% in the placebo group) but reduced hypokalemia.
26 human urine, the latter being diagnostic for hypokalemia.
27 e of electrolyte abnormalities, particularly hypokalemia.
28 atch-clamped ventricular myocytes exposed to hypokalemia (1.0-3.5 mmol/L) in the absence or presence
29 tion impairment (14.9%; 95% CI, 6.2%-28.3%), hypokalemia (11.9%; 95% CI, 3.9%-25.6%), hearing loss (1
30 a (29.0% v 34.5%), diarrhea (11.2% v 19.6%), hypokalemia (13.1% v 14.9%), anemia (13.9% v 13.6%), thr
32 nt-resistant hypertension, 6351 (43.5%) with hypokalemia, 1537 (10.5%) younger than 35 years, and 445
34 brile neutropenia (47% v 35%, respectively), hypokalemia (18% v 11%, respectively), thrombocytopenia
36 verload with BayK8644, and ionic stress with hypokalemia; 2), computer simulations using a physiologi
37 22% in arms A, B, and C, respectively), and hypokalemia (21%, 15%, and 5% in arms A, B, and C, respe
39 nd sustained vasodilation vs usual care were hypokalemia (23% vs 25%), worsening renal function (21%
40 was a high lactate level (48%), followed by hypokalemia (27.4%); 59 (58.2%) patients had hyperglycem
41 a (5.0% v 14.4%), stomatitis (1.3% v 13.6%), hypokalemia (3.6% v 10.8%), and treatment-related deaths
42 itis, palmar-plantar erythrodysesthesia, and hypokalemia (400 mg twice per day; n = 1); and grade 3 t
43 re anemia (64.8%), thrombocytopenia (62.0%), hypokalemia (49.3%), neutropenia (47.9%), and peripheral
46 patients), nausea (74.5%), vomiting (52.7%), hypokalemia (50.9%), and febrile neutropenia (45.5%).
49 or 2; the most frequent grade >/= 3 AEs were hypokalemia (8.9%), thrombocytopenia (8.0%), and fatigue
50 intravenous furosemide increases the risk of hypokalemia a especially when baseline K(+) is <=4.3 mmo
51 opic drugs are administered to patients with hypokalemia, abnormal T wave morphology, HCV infection,
52 stinal peptideoma [VIPoma], watery diarrhea, hypokalemia-achlorhydria [WDHA], glucagonoma [glucagonom
53 RG) Our results show that chronic hypoxia or hypokalemia additively reduced I(hERG) with fentanyl.
54 one were more likely to be hospitalized with hypokalemia (adjusted hazard ratio, 3.06 [CI, 2.04 to 4.
55 r more current antihypertensive medications; hypokalemia; age younger than 35 years; or adrenal nodul
57 imbalances, such as reduced serum K+ levels (hypokalemia), also trigger these potentially fatal arrhy
58 as no association between the development of hypokalemia and 30- and 90-day mortality and readmission
60 y, one must consider CF when confronted with hypokalemia and alkalosis in a previously healthy patien
64 treatment-emergent adverse events, including hypokalemia and elevated serum aminotransferases, were m
66 riables associated with risk of TdP included hypokalemia and female gender; by contrast, persistent a
67 sy-to-implement strategies to deal with both hypokalemia and hyperkalemia are provided as well as gui
70 Likewise, the adjusted hazard ratios for hypokalemia and hyperkalemia, normokalemia as reference,
73 ats and sudden death of transgenic mice with hypokalemia and imply that K2P1 leak cation channels may
74 e of spironolactone was associated with less hypokalemia and improved survival in patients with sever
75 rption in outer medullary collecting duct in hypokalemia and in acid-base regulation in conditions th
76 between pre-cardiac arrest hyperkalemia and hypokalemia and in-hospital cardiac arrest and outcomes
78 Key secondary outcomes were the incidence of hypokalemia and potassium reduction stratified by baseli
79 Concomitant magnesium deficiency aggravates hypokalemia and renders it refractory to treatment by po
80 enabled by membrane hyperpolarization during hypokalemia and short action potential configurations.
83 Long-term toxicities occurred in 2 patients: hypokalemia and tremor, both grade III, on days 370 and
93 evaluate the incidence and risk factors for hypokalemia, and its impact on mortality and readmission
94 ing duct of mouse kidney caused hypotension, hypokalemia, and metabolic alkalosis, an exact mirror im
97 A combination of bradycardic stimulation, hypokalemia, and quinidine resulted in early afterdepola
98 group (abdominal pain, diarrhoea, dyspnoea, hypokalemia, and respiratory failure), and four (15%) pa
100 characterized by acute attacks of weakness, hypokalemia, and thyrotoxicosis of various etiologies.
102 th a higher risk of an eating disorder were: hypokalemia (aOR, 1.98; 95% CI, 1.70-2.32), hyperkalemia
104 potassium levels and minimizing the risk of hypokalemia associated with other potassium control meas
108 everity was associated with injury severity, hypokalemia, baseline CIWA-Ar score, and established alc
109 pendently associated with the development of hypokalemia: baseline K(+) values (OR per 0.1 units, 0.8
110 electrolyte abnormalities (eg, hyponatremia, hypokalemia), bradycardia, disturbances in reproductive
112 nnels contribute to ectopic heartbeats under hypokalemia, by analysis of transgenic mice, which condi
114 y significant arrhythmias, and post-dialysis hypokalemia compared with hemodialysate potassium 2.0/no
115 se was also associated with a higher risk of hypokalemia compared with hydrochlorothiazide use, which
117 n isolated rat myocytes exposed to simulated hypokalemia conditions (reduction of extracellular [K(+)
119 s associated with secondary hypertension and hypokalemia, consistent with pseudohyperaldosteronism, a
120 d creatinine, or hyperkalemia (increased) or hypokalemia (decreased) related to finerenone did not di
121 constipation, febrile neutropenia, fatigue, hypokalemia, decreased appetite, and decreased white blo
124 less than 3.1 mEq/L and hospitalization for hypokalemia differed among those with and without prior
125 on is more effective in normokalemia than in hypokalemia due to the difference in dynamical threshold
127 nism in which NEDD4-2 deficiency exacerbates hypokalemia during dietary K(+) restriction primarily th
128 ill within the normal range and before frank hypokalemia ensues, in addition to the classic feedback
129 is dynamical threshold becomes much lower in hypokalemia, especially with respect to calcium, as pred
134 mer were more likely to be hospitalized with hypokalemia for all 6 comparisons in which a statistical
135 istically significant increased incidence of hypokalemia for chlorthalidone vs hydrochlorothiazide wa
136 de a strong diuretic regimen without causing hypokalemia for patients with fluid overload, including
140 g QT had significantly higher frequencies of hypokalemia, hepatitis C virus (HCV) infection, HIV infe
141 as abnormal test results for a composite of hypokalemia, hyperkalemia, hyponatremia, hypernatremia,
143 ded diarrhea, hypoalbuminemia, hyponatremia, hypokalemia, hypocalcemia, and hypomagnesemia; 14 patien
144 gation were female sex, QT-prolonging drugs, hypokalemia, hypocalcemia, hyperglycemia, high creatinin
145 f infusion-related reactions, renal failure, hypokalemia, hypomagnesemia, and anemia than patients in
146 ltiple time-points, and frequency of anemia, hypokalemia, hypomagnesemia, and liver toxicity were sim
147 The incidence of worsening kidney function, hypokalemia, hypotension, and adverse events was similar
148 and female survivors are fertile but exhibit hypokalemia, hypotonic polyuria, and apparent mineraloco
149 a resolution, at the risk of inducing severe hypokalemia in addition to hyponatremia, hypotension, an
151 nd K(+) balance and promotes hypotension and hypokalemia in response to Na(+) and K(+) depletion, res
153 d by various factors such as hyperkalemia or hypokalemia in the long term, or by delayed afterdepolar
154 oms or syndromes, including hypertension and hypokalemia (in patients with aldosteronoma), Cushing sy
155 ificant electrolyte disorders, mostly due to hypokalemia, in acutely ill children compared with previ
158 n diuretics are used; and (3) concerns about hypokalemia-induced arrhythmias have been overstated.
161 tion of Kir2.6 predisposes the sarcolemma to hypokalemia-induced paradoxical depolarization during at
162 inactive analogue KN-92, abolished EADs and hypokalemia-induced ventricular tachycardia/fibrillation
167 hen HCTZ is added to furosemide, the risk of hypokalemia is present with higher baseline K(+) values
170 ence and risk factors for the development of hypokalemia (K(+) <3.5 mmol/L) and its association with
171 d serum K(+) concentrations that occur under hypokalemia, K2P1 two-pore domain K(+) channels change i
172 significant electrolyte disorder, defined as hypokalemia less than 3.5 mmol/L, hypernatremia greater
174 LDO/salt + furosemide and was accompanied by hypokalemia (<3.4 mmol/l) that were rescued by spironola
175 t common gastrointestinal adverse event, and hypokalemia (<3.5 mEq/L) occurred in 5.6% of patients.
179 ive haemorrhage in basal ganglia and chronic hypokalemia-mediated nephrocalcinosis and renal cysts.
180 ntal retardation, and electrolyte imbalance (hypokalemia, metabolic alkalosis, and hypomagnesemia).
181 autoimmune thrombocytopenia (n = 1; 2%), and hypokalemia (n = 1; 2%), which resolved spontaneously or
182 entified: heart failure (n=8), angina (n=2), hypokalemia (n=1), adverse antiarrhythmic drug treatment
183 ypercalcemia at 15 mg/m(2); hypophosphatemia/hypokalemia, neutropenia, and somnolence at 40 mg/m(2);
186 % (SZC) and 37.6% (placebo) of participants; hypokalemia occurred in 3.0% (SZC) and 1.4% (placebo).
193 ated by certain conditions, such as hypoxia, hypokalemia, or alkalosis, which may increase the risk o
196 e that Na-K pump inhibition by even moderate hypokalemia plays a critical role in promoting EAD-media
198 f hyperkalemia (potassium >/=5.5 mmol/L) and hypokalemia (potassium <3.5 mmol/L) and the relationship
199 utcomes included achieved blood pressure and hypokalemia (potassium level <3.1 mEq/L; to convert to m
200 tted to the study on the basis of documented hypokalemia (potassium of < 3.5 mmol/L) within the 24-hr
201 us 4.2%; P<0.046), as well as lower rates of hypokalemia (potassium<3.5 mmol/L; 5.6% versus 17.9%; P<
202 laxative use with risk of dyskalemia (i.e., hypokalemia [potassium <3.5 mEq/L] or hyperkalemia [>5.5
203 h severe hypoglycemia; 2) with limitation of hypokalemia, potassium supplementation could limit hypog
204 6045 [3.4%] [P < .001]; hospitalization for hypokalemia: prior MI or stroke, 14 of 733 [1.9%] vs 16
205 This observation provides insight into why hypokalemia promotes calcium-mediated triggered activity
210 tubulopathy characterized by hypomagnesemia, hypokalemia, salt wasting, and nephrocalcinosis, we iden
212 id-suppressible hyperaldosteronism may cause hypokalemia, suppressed plasma renin activity, and hyper
213 served that the stimulus needed was lower in hypokalemia than in normokalemia in both computer simula
214 ver, the mechanism of renal K(+) wasting and hypokalemia that develop in individuals with ROMK Bartte
216 ngly with the severity of DKA, the degree of hypokalemia, the presence of complications, and admissio
217 y NaCl wasting, and metabolic alkalosis with hypokalemia, thereby recapitulating the phenotype of Bar
218 e of the patients reported CTC grades 3 to 4 hypokalemia, three reported CTC grade 3 acute renal inju
219 exposed to either oxidative stress (H2O2) or hypokalemia to induce bradycardia-dependent EADs at a lo
221 placebo group (P=0.002), whereas the rate of hypokalemia was 8.4 percent in the eplerenone group and
223 um tremens (odds ratio, 6.08; p = 0.01), and hypokalemia was borderline significant (odds ratio, 3.23
226 doubling of creatinine were more likely and hypokalemia was less likely in patients receiving spiron
228 Ca(2+)-dependent spontaneous activity during hypokalemia was only observed in a minority of atrial ce
234 orticoid-related toxicities (hypertension or hypokalemia) was reduced by adding low-dose prednisone.
236 ytopenia, abnormal liver function tests, and hypokalemia were reported more often for SRL-ST therapy.
237 reactions (mainly hypotension, flushing, and hypokalemia) were self-limiting and not higher than grad
238 including fluid retention, hypertension, and hypokalemia, were more frequently reported in the abirat
239 eated with furosemide alone a higher risk of hypokalemia when baseline K(+) values are <=3.7 mmol/L.
242 ial depolarization, hearts were subjected to hypokalemia, which had no effect in wild-type hearts but
243 nal failure, and metabolic alkalosis without hypokalemia, which were all corrected with salt replacem
246 elman-like syndrome (fortuitous discovery of hypokalemia with hypomagnesemia and/or hypocalciuria in
248 with HF exhibited less hyperkalemia and more hypokalemia with spironolactone compared with non-AAs an
249 ter modeling revealed that EAD generation by hypokalemia (with or without dofetilide) required Na-K p