ライフサイエンスコーパス: loop diuretic

1 and treatment with an antiarrythmics drug or loop diuretic).

2 ion fraction <35%, and use of eplerenone and loop diuretic.

3 ulation of blood pressure, and response to a loop diuretic.

4 a novel approach to potentiate the action of loop diuretics.

5 ailure management, typically addressed using loop diuretics.

6 fluid overload despite significant doses of loop diuretics.

7 it is the target of the clinically important loop diuretics.

8 level and are pharmacologically inhibited by loop diuretics.

9 >/=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

10 line characteristics, cumulative in-hospital loop diuretic administered, and worsening of renal funct

11 sodium handling, to assess sodium exit after loop diuretic administration and FENa to assess the net

12 pot urine sample obtained 1 or 2 hours after loop diuretic administration.

13 slocation rate, apparent ion affinities, and loop diuretic affinity, consistent with a proposed role

14 mally acting agents (e.g., acetazolamide and loop diuretic agents) are preferred.

15 in 5,864 subjects; of these, 5,320 received loop diuretics and had dose data recorded.

16 eceptor antagonist, enhances the response to loop diuretics and may have a renal protective effect.

17 n angiotensin-converting-enzyme inhibitor, a loop diuretic, and in most cases digoxin.

18 ricosuric, nonsteroidal anti-inflammatories, loop diuretics, angiotensin II receptor antagonists, and

19 Hypersensitivity to thiazide and loop diuretics, angiotensin-converting enzyme inhibitors

20 Loop diuretics are an essential component of therapy for

21 Loop diuretics are commonly used to control congestive s

22 Intravenous loop diuretics are the mainstay of therapy for patients

23 ggest a role for neurohormonal activation in loop diuretic-associated mortality.

24 cker Evaluation of Survival Trial) receiving loop diuretics at baseline were analyzed (N = 2,456).

25 luded: (1) observational: patients receiving loop diuretics at the Yale Transitional Care Center (N=1

26 nts with HF (n=128) receiving treatment with loop diuretics at the Yale Transitional Care Center.

27 and VIP+ neurons-a low concentration of the loop diuretic bumetanide had differential effects on AVP

28 sses, and pharmacologic inhibition using the loop diuretic bumetanide inhibits in vitro Transwell mig

29 Since NKCC2 is the molecular target of the loop diuretics bumetanide and furosemide, we asked about

30 Preclinical data suggest that the loop-diuretic bumetanide might be an effective treatment

31 Binding of loop diuretics can curtail their action in the loop of H

32 d a longer median time to the second dose of loop diuretics compared with long call patients (17.9 ho

33 Rodents chronically administered loop diuretics develop DR due to compensatory distal tub

34 se the formation of mineralized nodules, but loop diuretics do not.

35 ntion strategies (atrial natriuretic factor, loop diuretics, dopamine, mannitol) have shown no clear

36 Loop diuretic dose (furosemide equivalent) was 80 (40, 1

37 y hemoconcentration had higher average daily loop diuretic doses (p = 0.001), greater weight loss (p

38 Loop diuretic doses were on averaged doubled during the

39 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

40 osemide, consistent with the hypothesis that loop diuretic drugs bind within the translocation cavity

41 me, a disease that mimics the effects of the loop diuretic furosemide, ClC-Kb/K2 is assumed to have a

42 ypotonic conditions, and is inhibited by the loop diuretic furosemide.

43 e of this study was to determine whether the loop diuretics furosemide, bumetanide and ethacrynic aci

44 ears (HR: 1.05, 95% CI: 0.51 to 2.17), daily loop diuretic, furosemide equivalents >240 mg (HR: 1.49,

45 cute decompensated heart failure (ADHF), and loop diuretics have historically been the cornerstone of

46 utcomes associated with the use of high-dose loop diuretics (HDLD).

47 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

48 netic ablation of claudin-14 or the use of a loop diuretic in mice abrogated HDAC inhibitor-induced h

49 The demonstrated efficacy of loop diuretics in managing congestion is balanced by the

50 gs of our study demonstrate increased use of loop diuretics in patients with BP before the developmen

51 Response to loop diuretics in patients with nephrotic syndrome (NS)

52 regulate osmotic stability are disrupted by loop diuretics in rats.

53 ot analysis of NCC protein demonstrated that loop diuretics increased NCC protein abundance by nearly

54 d timed 6-hour urine collections to quantify loop diuretic-induced cumulative sodium output.

55 e that increased NCC activity during chronic loop diuretic infusion is associated with increases in N

56 designed to test the hypotheses that chronic loop diuretic infusion, with replacement of NaCl losses,

57 es for TM3 residues in ion translocation and loop diuretic inhibition.

58 Chronic infusion of loop diuretics into animals induces structural and funct

59 Coadministration of BNP and loop diuretic is effective in maximizing natriuresis and

60 is concluded that urinary protein binding of loop diuretics is not a major mechanism for the diuretic

61 When administration of moderate doses of loop diuretics is not sufficient, patients can be treate

62 Furosemide, a loop diuretic, is commonly used in patients with congest

63 g hemoconcentration received higher doses of loop diuretics, lost more weight/fluid, and had greater

64 e, administration of mixtures of albumin and loop diuretics may enhance responses.

65 cs: heart failure on problem list, inpatient loop diuretic, or brain natriuretic peptide level of 500

66 Loop diuretics other than furosemide were converted to f

67 ation of the use of a nonrenally metabolized loop diuretic rather than furosemide.

68 n can increase the volume of distribution of loop diuretics, reduce their tubular secretion, and enha

69 One approach to overcome loop diuretic resistance is the addition of a thiazide-t

70 ot using a thiazide diuretic, or not using a loop diuretic, respectively.

71 Strategies to improve loop diuretic responsiveness include increasing diuretic

72 rs, beta-blockers, calcium channel blockers, loop diuretics, selective serotonin reuptake inhibitors,

73 loride cotransporter gene family, including "loop" diuretic-sensitive Na-K-Cl cotransport and thiazid

74 Vasopressin receptor antagonists, urea, and loop diuretics serve this purpose, but received differen

75 gy of the K-Cl cotransporter is dominated by loop diuretics such as furosemide and bumetanide, molecu

76 All three loop diuretics suppressed sound-triggered seizures in po

77 a putative drug target for a novel class of loop diuretic that would lower blood volume and pressure

78 vaptan may allow for less intensification of loop diuretic therapy and a lower incidence of worsening

79 atients otherwise resistant to high doses of loop diuretics, this strategy has not been subjected to

80 ata suggest that administration of high-dose loop diuretics to patients with HF yields meaningful inc

81 otensin converting enzyme (ACE) inhibitor or loop diuretics to those 75 years or older without assess

82 Thiazide and loop diuretics were associated with higher risk of incid

83 Thiazide and loop diuretics were associated with increased gout risk,

84 ms, and scheduled treatment with intravenous loop diuretics were included.

85 Loop diuretics were used significantly more frequently b

86 ma (0.73, 0.58-0.91); or an ACE inhibitor or loop diuretic without appropriate monitoring (0.51, 0.34