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1 and treatment with an antiarrythmics drug or loop diuretic).
2 tion rate and were more often treated with a loop diuretic.
3 urinary sodium when used in combination with loop diuretic.
4 ion fraction <35%, and use of eplerenone and loop diuretic.
5 ulation of blood pressure, and response to a loop diuretic.
6 level and are pharmacologically inhibited by loop diuretics.
7 iabetes mellitus and 96 (60%) were receiving loop diuretics.
8 adults with cardiovascular disease or taking loop diuretics.
9 andard decongestive treatments that included loop diuretics.
10 evidence of treatment effect modification by loop diuretics.
11 eart failure recorded but were not receiving loop diuretics.
12 and prevent congestion has historically been loop diuretics.
13 de or matching placebo on top of intravenous loop diuretics.
14 de or matching placebo on top of intravenous loop diuretics.
15 he molecular mechanisms of its inhibition by loop diuretics.
16  was stratified according to previous use of loop diuretics.
17 a novel approach to potentiate the action of loop diuretics.
18  effect of empagliflozin in combination with loop diuretics.
19 ailure management, typically addressed using loop diuretics.
20  fluid overload despite significant doses of loop diuretics.
21 inical outcomes than those not discharged on loop diuretics.
22 it is the target of the clinically important loop diuretics.
23 sts (0.69 [0.50-0.96], 0.48 [0.35-0.66]), or loop diuretics (0.67 [0.53-0.85], 0.45 [0.37-0.55]).
24 >/=2 QT-prolonging drugs (2.6 [1.9-5.6]), or loop diuretic (1.4 [1.0-2.0]), age >68 years (1.3 [1.0-1
25 y higher for heart failure in the absence of loop diuretics [22%; adjHR 1.2 (95% CI 1.1-1.3)], substa
26 ection fraction of <40% (7.7%), or were on a loop diuretic (29.9%).
27 etic Resistance cohort receiving intravenous loop diuretics (462 administrations in 285 patients) und
28 , and highest for heart failure treated with loop diuretics [52%; adjHR 2.2 (95% CI 2.0-2.2)].
29 s on loop diuretics compared to those not on loop diuretics (adjusted mean difference vs. placebo: +9
30 line characteristics, cumulative in-hospital loop diuretic administered, and worsening of renal funct
31 sodium handling, to assess sodium exit after loop diuretic administration and FENa to assess the net
32 sing a spot urine sample collected 2 h after loop diuretic administration.
33 pot urine sample obtained 1 or 2 hours after loop diuretic administration.
34                               Evaluating 638 loop diuretic administrations, the NRPE showed excellent
35 slocation rate, apparent ion affinities, and loop diuretic affinity, consistent with a proposed role
36 re likely to be treated with high doses of a loop diuretic agent as an outpatient (all p < 0.001).
37 eart Association class at randomization, and loop diuretic agent before hospitalization.
38 iltration rate, and fewer new initiations of loop diuretic agent therapy.
39 ie, adding a second-line diuretic agent to a loop diuretic agent, should be reserved for those patien
40 mally acting agents (e.g., acetazolamide and loop diuretic agents) are preferred.
41 mptoms and congestion can be controlled with loop diuretic agents, the main focus should be rapid gui
42 ts as much as possible with diuretic agents (loop diuretic agents, thiazides, acetazolamide) or mecha
43 ved for those patients who do not respond to loop diuretic agents.
44 ) and 6.6% (144 of 2,191) of patients in the loop diuretic and no loop diuretic groups, respectively
45 dy was to determine the relationship between loop diuretics and clinical outcomes in patients with HF
46  in 5,864 subjects; of these, 5,320 received loop diuretics and had dose data recorded.
47 eceptor antagonist, enhances the response to loop diuretics and may have a renal protective effect.
48      Second-line therapeutic options include loop diuretics and salt tablets, urea, and V2 receptor a
49 gets of clinically important drugs including loop diuretics and their disruption has been implicated
50  or more, and 2 doses or more of intravenous loop diuretics and/or new hemodialysis or continuous kid
51 re on no diuretic, 769 (12.3%) were on a non-loop diuretic, and 4811 (76.8%) were on a loop diuretic
52 Association Class III or IV, nearly all on a loop diuretic, and 70% with a HF hospitalization in the
53 n angiotensin-converting-enzyme inhibitor, a loop diuretic, and in most cases digoxin.
54 in the following subgroups: no diuretic, non-loop diuretic, and loop diuretic furosemide equivalent d
55 844 (4%) had heart failure recorded and took loop diuretics, and 5156 (3%) had heart failure recorded
56 ricosuric, nonsteroidal anti-inflammatories, loop diuretics, angiotensin II receptor antagonists, and
57             Hypersensitivity to thiazide and loop diuretics, angiotensin-converting enzyme inhibitors
58                                              Loop diuretics are a primary therapy for the symptomatic
59                                              Loop diuretics are an essential component of therapy for
60                                              Loop diuretics are commonly used to control congestive s
61  for the management of hypertension, whereas loop diuretics are often needed for volume overload, whi
62                                              Loop diuretics are one of the cornerstones of treatments
63                                  Intravenous loop diuretics are the mainstay of therapy for patients
64                                              Loop diuretics are used for congestion relief, and dose
65 th are its cardinal manifestations for which loop diuretics are used.
66 r type 2 inhibitors, exercise, HF self-care, loop diuretics as needed to maintain euvolemia, and weig
67 o eplerenone would lead clinicians to reduce loop diuretics, as a consequence of the improvement in p
68 ggest a role for neurohormonal activation in loop diuretic-associated mortality.
69 on-loop diuretic, and 4811 (76.8%) were on a loop diuretic at baseline.
70 cker Evaluation of Survival Trial) receiving loop diuretics at baseline were analyzed (N = 2,456).
71 pronounced benefits among patients receiving loop diuretics at baseline.
72  achieved despite a lower mean daily dose of loop diuretics at day 90 in the HIC arm.
73  7,936 patients, 5,568 (70%) were prescribed loop diuretics at discharge.
74 luded: (1) observational: patients receiving loop diuretics at the Yale Transitional Care Center (N=1
75 nts with HF (n=128) receiving treatment with loop diuretics at the Yale Transitional Care Center.
76 or placebo added to standardized intravenous loop diuretics (at a dose equivalent to twice the oral m
77  and VIP+ neurons-a low concentration of the loop diuretic bumetanide had differential effects on AVP
78 sses, and pharmacologic inhibition using the loop diuretic bumetanide inhibits in vitro Transwell mig
79   Since NKCC2 is the molecular target of the loop diuretics bumetanide and furosemide, we asked about
80            Preclinical data suggest that the loop-diuretic bumetanide might be an effective treatment
81 hNKCC1), both in the absence and presence of loop diuretic (bumetanide or furosemide), using single-p
82  (reference group), 23 963 (12%) were taking loop diuretics but had no heart failure recorded, 7844 (
83 nhibitors will likely be coprescribed with a loop diuretic, but this combined effect is not well-defi
84      Dapagliflozin reduced new initiation of loop diuretics by 32% [hazard ratio (HR) 0.68; 95% confi
85                                   Binding of loop diuretics can curtail their action in the loop of H
86 score improvement was greater in patients on loop diuretics compared to those not on loop diuretics (
87 d a longer median time to the second dose of loop diuretics compared with long call patients (17.9 ho
88             Rodents chronically administered loop diuretics develop DR due to compensatory distal tub
89 te medication data and who were prescribed a loop diuretic, diuretic dose increase was defined as: (1
90 se the formation of mineralized nodules, but loop diuretics do not.
91 ntion strategies (atrial natriuretic factor, loop diuretics, dopamine, mannitol) have shown no clear
92                                              Loop diuretic dose (furosemide equivalent) was 80 (40, 1
93 etic use categories (Pinteraction = 0.64) or loop diuretic dose (Pinteraction = 0.57).
94 weight loss (WL), WL adjusted for mean daily loop diuretic dose (WL-adjusted), area under the curve o
95 rics of disease severity such as higher home loop diuretic dose and NT-proBNP (N-terminal pro-B-type
96 -9.1, -4.7] from no diuretics to the highest loop diuretic dose category; interaction P = .39).
97                   From baseline to 52 weeks, loop diuretic dose decreased by 17% in the semaglutide g
98                              First sustained loop diuretic dose increases were less frequent, and sus
99        placebo) was more likely to result in loop diuretic dose reduction (odds ratio [OR] 2.67 [95%
100                Eplerenone treatment led to a loop diuretic dose reduction during follow-up without ev
101 ity and mortality regardless of the baseline loop diuretic dose used: hazard ratio for the outcome of
102 tion (NRPE) predicts natriuresis following a loop diuretic dose using a urine sample 2 h after the do
103 d as cumulative weight change per cumulative loop diuretic dose, was compared across treatment assign
104 -hour urine volume, and percentage change in loop diuretic dose.
105 g placebo on top of standardized intravenous loop diuretics (dose equivalent of twice oral maintenanc
106    Dapagliflozin was associated with reduced loop diuretic doses (560 mg [Q1-Q3: 260-1,150 mg] vs 800
107 y hemoconcentration had higher average daily loop diuretic doses (p = 0.001), greater weight loss (p
108 eatment was associated with lower prescribed loop diuretic doses throughout the follow-up; lower dose
109      Both baseline and follow-up incremental loop diuretic doses were associated with worse prognosis
110                                              Loop diuretic doses were on averaged doubled during the
111 symptoms, which enables clinicians to reduce loop diuretic doses.
112 VR 0.81, 95% CI 0.76-0.86, p<0.0001) and non-loop diuretic drugs (0.87, 0.79-0.96, p=0.007), and incr
113 osemide, consistent with the hypothesis that loop diuretic drugs bind within the translocation cavity
114 e in pulmonary congestion (lung ultrasound), loop diuretic efficiency (weight change per 40 mg of fur
115 ion, cumulative urine and sodium output, and loop diuretic efficiency [P 0.33 for all]) or neurohormo
116                                              Loop diuretic efficiency was less with dapagliflozin tha
117       Using propensity scores for receipt of loop diuretics estimated for each of the 7,936 patients,
118        Participants received their home oral loop diuretic followed by a supervised timed urine colle
119 thy, combination aldosterone antagonists and loop diuretics for ascites, and terlipressin for hepator
120 bgroups: no diuretic, non-loop diuretic, and loop diuretic furosemide equivalent doses of <40, 40, an
121 me, a disease that mimics the effects of the loop diuretic furosemide, ClC-Kb/K2 is assumed to have a
122 ypotonic conditions, and is inhibited by the loop diuretic furosemide.
123 e of this study was to determine whether the loop diuretics furosemide, bumetanide and ethacrynic aci
124 ), both in the absence and presence of bound loop diuretic (furosemide or bumetanide).
125  includes escalation or trial of intravenous loop diuretics (furosemide or bumetanide) in bolus (2-3
126 ears (HR: 1.05, 95% CI: 0.51 to 2.17), daily loop diuretic, furosemide equivalents >240 mg (HR: 1.49,
127                             Treatment with a loop diuretic, furosemide, under insulinopenic condition
128                              Patients in the loop diuretic group had a significantly lower risk of 30
129 191) of patients in the loop diuretic and no loop diuretic groups, respectively (HR when the use of l
130 on who received a discharge prescription for loop diuretics had significantly better 30-day clinical
131 cute decompensated heart failure (ADHF), and loop diuretics have historically been the cornerstone of
132                                              Loop diuretics have well-described toxicities, and loss
133 utcomes associated with the use of high-dose loop diuretics (HDLD).
134 diuretic (HR 1.44 [95% CI 1.00, 2.10]), or a loop diuretic (HR 2.31 [95% CI 1.36, 3.91]) was associat
135 netic ablation of claudin-14 or the use of a loop diuretic in mice abrogated HDAC inhibitor-induced h
136 lthough furosemide is the most commonly used loop diuretic in patients with heart failure, some studi
137 diuretics are considered less effective than loop diuretics in CKD.
138                 The demonstrated efficacy of loop diuretics in managing congestion is balanced by the
139            Effective diuretic regimens using loop diuretics in patients with acute decompensated hear
140                 When added to treatment with loop diuretics in patients with acute decompensated HF,
141 gs of our study demonstrate increased use of loop diuretics in patients with BP before the developmen
142                                  Response to loop diuretics in patients with nephrotic syndrome (NS)
143  regulate osmotic stability are disrupted by loop diuretics in rats.
144  transporters are inhibited by the so-called loop diuretics including bumetanide, and these drugs are
145                                              Loop diuretics, including furosemide, bumetanide, and to
146                             The mean dose of loop diuretic increased over time in the placebo arm, a
147 ot analysis of NCC protein demonstrated that loop diuretics increased NCC protein abundance by nearly
148 d timed 6-hour urine collections to quantify loop diuretic-induced cumulative sodium output.
149 se is magnified in patients with baseline or loop diuretic-induced elevated HCO3 (marker of proximal
150 uretic sodium reabsorption (CPDSR) following loop diuretic-induced natriuresis, minimizing sodium exc
151 e that increased NCC activity during chronic loop diuretic infusion is associated with increases in N
152 designed to test the hypotheses that chronic loop diuretic infusion, with replacement of NaCl losses,
153 es for TM3 residues in ion translocation and loop diuretic inhibition.
154 utpatient worsening heart failure (HF) (oral loop diuretic intensification or initiation) is simple t
155                          Chronic infusion of loop diuretics into animals induces structural and funct
156                  Coadministration of BNP and loop diuretic is effective in maximizing natriuresis and
157 is concluded that urinary protein binding of loop diuretics is not a major mechanism for the diuretic
158     When administration of moderate doses of loop diuretics is not sufficient, patients can be treate
159                                Furosemide, a loop diuretic, is commonly used in patients with congest
160 g hemoconcentration received higher doses of loop diuretics, lost more weight/fluid, and had greater
161  220), non-loop diuretic only (n = 223), and loop diuretic [&lt;40 (n = 219), 40 (n = 309), and >40 (n =
162              There was no difference in mean loop diuretic management (daily furosemide equivalents)
163  over time and appeared to be independent of loop diuretic management.
164 e, administration of mixtures of albumin and loop diuretics may enhance responses.
165 nd tended to be discharged on lower doses of loop diuretic (mean [SD], 50.3 [46.2] mg vs 63.8 [52.4]
166 ted in two HF patient cohorts receiving oral loop diuretics: Mechanisms of Diuretic Resistance (MDR)
167 events the drop in chloride levels caused by loop diuretic monotherapy.
168 ears; 55% women), 161 935 (81%) neither took loop diuretics nor had a diagnostic record of heart fail
169  baseline, across no diuretic (n = 220), non-loop diuretic only (n = 223), and loop diuretic [<40 (n
170                                            A loop diuretic only strategy was associated with an incre
171 ed decongestive response in the placebo arm (loop diuretics only), both with regard to reaching the p
172 cs: heart failure on problem list, inpatient loop diuretic, or brain natriuretic peptide level of 500
173                                              Loop diuretics other than furosemide were converted to f
174  reabsorption, can improve the efficiency of loop diuretics, potentially leading to more and faster d
175 ys between first HF hospitalization or first loop diuretic prescription and ATTR-CM diagnosis.
176                For the 1,882 veterans with a loop diuretic prescription before ATTR-CM diagnosis, the
177 nsional setting identified patients with >=2 loop diuretic prescriptions (aRD, -2.6%, 95% CI, -5.0% t
178 ation of the use of a nonrenally metabolized loop diuretic rather than furosemide.
179 n can increase the volume of distribution of loop diuretics, reduce their tubular secretion, and enha
180 with dapagliflozin significantly reduced new loop diuretic requirement over time.
181                     One approach to overcome loop diuretic resistance is the addition of a thiazide-t
182           In patients with heart failure and loop diuretic resistance, dapagliflozin was not more eff
183 ot using a thiazide diuretic, or not using a loop diuretic, respectively.
184                        Strategies to improve loop diuretic responsiveness include increasing diuretic
185 natriuresis, particularly when combined with loop diuretics, resulting in an improvement in blood vol
186 rs, beta-blockers, calcium channel blockers, loop diuretics, selective serotonin reuptake inhibitors,
187 loride cotransporter gene family, including "loop" diuretic-sensitive Na-K-Cl cotransport and thiazid
188  Vasopressin receptor antagonists, urea, and loop diuretics serve this purpose, but received differen
189                                              Loop diuretic strategy of torsemide (n = 1431) or furose
190 s were randomly assigned in a 1:1 ratio to a loop diuretic strategy of torsemide or furosemide with i
191 ategorized by HF type and further divided by loop diuretic strategy.
192 gy of the K-Cl cotransporter is dominated by loop diuretics such as furosemide and bumetanide, molecu
193 c effect, a common liability associated with loop diuretics such as furosemide.
194                         Diuretics (typically loop diuretics, such as furosemide or torsemide) should
195                                              Loop diuretics, such as furosemide, torsemide, and bumet
196                                    All three loop diuretics suppressed sound-triggered seizures in po
197  a putative drug target for a novel class of loop diuretic that would lower blood volume and pressure
198                               Treatment with loop diuretics, the current cornerstone of decongestive
199 vaptan may allow for less intensification of loop diuretic therapy and a lower incidence of worsening
200             The addition of acetazolamide to loop diuretic therapy in patients with acute decompensat
201 atients otherwise resistant to high doses of loop diuretics, this strategy has not been subjected to
202 y (YDP) cohort, which used the NRPE to guide loop diuretic titration via a nurse-driven automated pro
203 ata suggest that administration of high-dose loop diuretics to patients with HF yields meaningful inc
204 otensin converting enzyme (ACE) inhibitor or loop diuretics to those 75 years or older without assess
205 cebo in addition to standardized intravenous loop diuretics (twice that of the oral home maintenance
206 toclopramide, domperidone, anticholinergics, loop diuretics, urologics, and ophthalmics.
207       Semaglutide also led to a reduction in loop diuretic use and dose between baseline and 52 weeks
208 use, as well as the effect of semaglutide on loop diuretic use and dose changes over the 52-week trea
209 short-term clinical benefits associated with loop diuretic use in HF.
210 s similar to heart failure, or inappropriate loop diuretic use increases mortality; all might be true
211 sis of heart failure may be often missed, or loop diuretic use is associated with other conditions wi
212   Mortality is more strongly associated with loop diuretic use than with a record of heart failure.
213 ar regardless of ejection fraction, previous loop diuretic use, and baseline health status.
214 tic groups, respectively (HR when the use of loop diuretics was compared with nonuse: 0.73; 95% CI: 0
215                                 Thiazide and loop diuretics were associated with higher risk of incid
216                                 Thiazide and loop diuretics were associated with increased gout risk,
217 ms, and scheduled treatment with intravenous loop diuretics were included.
218 tion, combination aldosterone antagonist and loop diuretics were more likely to resolve ascites (76%
219                                              Loop diuretics were used significantly more frequently b
220 he NRPE to predict 6-h sodium output after a loop diuretic, which was defined as poor (<50 mmol), sub
221  circulating blood decreases with the use of loop diuretics, which might result in less immediate tra
222 ith reduced ejection fraction taking regular loop diuretic who were randomized to empagliflozin 25 mg
223 1.3)], substantially higher for those taking loop diuretics with no record of heart failure [40%; adj
224 ma (0.73, 0.58-0.91); or an ACE inhibitor or loop diuretic without appropriate monitoring (0.51, 0.34
225                 Many patients are prescribed loop diuretics without a diagnostic record of heart fail
226  cardiovascular disease, many are prescribed loop diuretics without a recorded diagnosis of heart fai

 
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