ライフサイエンスコーパス: diuretic

1 reatment with an antiarrythmics drug or loop diuretic).

2 t three antihypertensive agents, including a diuretic).

3 ihypertensive medications, one of which is a diuretic.

4 ng hospitalization or outpatient intravenous diuretic.

5 were on >/=2 classes and only 29% were on a diuretic.

6 d doses of at least three drugs, including a diuretic.

7 neys can produce urine after a given dose of diuretic.

8 difficult and there is need for a uricosuric diuretic.

9 raction <35%, and use of eplerenone and loop diuretic.

10 s with hypertension; 37% were treated with a diuretic.

11 ertensive patients who need treatment with a diuretic.

12 c shock includes inotropes, vasopressors and diuretics.

13 thier patients are simply more responsive to diuretics.

14 was confirmed by the natriuretic response to diuretics.

15 aemia may lead to the creation of uricosuric diuretics.

16 imilar after the exclusion of individuals on diuretics.

17 es of GS with a blunted response to thiazide diuretics.

18 blockers, angiotensin receptor blockers, and diuretics.

19 estinal bleeding, and patients that required diuretics.

20 ir actions on glycemic control or as osmotic diuretics.

21 el approach to potentiate the action of loop diuretics.

22 QT-prolonging drugs (2.6 [1.9-5.6]), or loop diuretic (1.4 [1.0-2.0]), age >68 years (1.3 [1.0-1.9]),

23 sive drug than in those receiving a thiazide diuretic (-2.38 mm Hg [-6.16 to 1.40]).

24 therapy (23.0% vs. 4.9% and 9.2%, p mu .01), diuretics (4.2% vs. 2.6% and 0.8%, p mu .001), or vasopr

25 domized patients (n=8399)were treated with a diuretic (80%) and beta-blocker (93%); 47% of those taki

26 At randomization, patients were receiving diuretics (95.9%), beta-blockers (82.5%), angiotensin-co

27 w ascites and peripheral edema, treated with diuretics, a low-salt diet, and fluid restriction.

28 for a particular drug (PPIs, NSAIDs, SSRIs, diuretics, ACE inhibitors) in the 6 months prior to the

29 Therefore, the diuretic action of kinin in Drosophila can be explained

30 The results provide proof of concept for the diuretic action of UT-A-selective inhibitors.

31 nolactone would therefore be superior to non-diuretic add-on drugs at lowering blood pressure.

32 characteristics, cumulative in-hospital loop diuretic administered, and worsening of renal function.

33 m handling, to assess sodium exit after loop diuretic administration and FENa to assess the net sodiu

34 benefits compared with those of traditional diuretic administration are unknown.

35 d and require a delay of several hours after diuretic administration before they are available.

36 Radiotracer T1/2 values after diuretic administration did not correlate with median SW

37 ll as change in median SWS (median SWS after diuretic administration minus median SWS before diuretic

38 iuretic response can be predicted soon after diuretic administration with excellent accuracy using a

39 retic administration minus median SWS before diuretic administration) were correlated with the amount

40 .08, P = .53) or after (r = -0.0004, P >.99) diuretic administration, nor did they correlate with int

41 ent by submitting mice to water deprivation, diuretic administration, or high-Na(+) diet increased re

42 ith improved clinical outcomes compared with diuretic administration.

43 rine sample obtained 1 or 2 hours after loop diuretic administration.

44 tion rate, apparent ion affinities, and loop diuretic affinity, consistent with a proposed role of TM

45 full-dose antihypertensive drugs including a diuretic agent or >/=4 drugs): control (ABP <125/75 mm H

46 least 3 antihypertensive drugs, including a diuretic agent.

47 We compared HFrEF patients treated with diuretic agents alone to three treatment arms: 1) ACEI t

48 t impair this mechanism (e.g., thiazide-type diuretic agents and mineralocorticoid receptor antagonis

49 Thiazide and thiazide-like diuretic agents are being increasingly used at lower dos

50 ephron segments with low water permeability, diuretic agents that impair this mechanism (e.g., thiazi

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

52 In contrast, compared with diuretic agents, some data suggest that adjustment of ul

53 The former is caused by diuretic agents, which enhance sodium excretion, often w

54 ts presenting with AHF requiring intravenous diuretic agents.

55 ty, electrolyte content, and the presence of diuretic agents.

56 d patients with AHF treated with intravenous diuretic agents.

57 class, diastolic blood pressure, and use of diuretic agents.

58 EI and ACEI+BB cohorts compared to that with diuretics alone were $444 and $33, respectively.

59 AHF therapies, such as diuretics, alter chloride homeostasis.

60 ition or substitution of a potassium-sparing diuretic, amiloride, to treatment with a thiazide can pr

61 The combination of a diuretic and an angiotensin receptor blocker (ARB) or an

62 less than 140/90 mmHg with a combination of diuretic and an ARB or ACEI.

63 Perhaps more important are the osmotic diuretic and natriuretic effects contributing to plasma

64 idone is a potent, long-acting thiazide-like diuretic and should be used preferentially to treat resi

65 artery pressure information, more changes in diuretic and vasodilator therapies were made in the trea

66 Beneficiaries initiating diuretics and beneficiaries initiating digoxin were more

67 d LVSD therapies (neurohormonal antagonists, diuretics and cardiac resynchronization in appropriate c

68 ,864 subjects; of these, 5,320 received loop diuretics and had dose data recorded.

69 ss by exercise training, sodium retention by diuretics and monitoring devices, myocardial nitric oxid

70 nd may be responsible for both resistance to diuretics and to endogenous natriuretic peptides.

71 summarizes available data on the use of both diuretics and UF in ADHF patients and identifies challen

72 in 11 patients we withdrew beta-blockers and diuretics and used phenylephrine and albumin infusion to

73 Despite inpatient diuretics and vasodilators targeting decongestion, persi

74 uncontrolled hypertension (P=0.049), need of diuretics, and age <60 years (P=0.016) were associated w

75 mic beta blockers, calcium channel blockers, diuretics, and angiotensin receptor antagonists), smokin

76 et agents, warfarin, statins, beta-blockers, diuretics, and antiarrhythmic drugs.

77 A low eGFR, age <60 years, need of diuretics, and uncontrolled hypertension identify patien

78 uric, nonsteroidal anti-inflammatories, loop diuretics, angiotensin II receptor antagonists, and beta

79 y used antihypertensive medications included diuretics, angiotensin-converting enzyme inhibitors (ACE

80 We show that the diuretic, anti-hypertensive, AMPA receptor modulator cyc

81 family, used in traditional medicine for its diuretic, antipyretic, diaphoretic, antispasmodic, tonic

82 Thiazide diuretics are among the most commonly prescribed antihyp

83 Thiazide diuretics are among the most widely used treatments for

84 Thiazide-type diuretics are associated with an increased incidence of

85 Diuretics are commonly used to treat hypertension and ex

86 Diuretics are used to decongest patients; however, morta

87 Thiazide diuretics are used to treat hypertension; however, compe

88 ntly better than thiazides and thiazide-like diuretics as a first-line therapy for any outcome.

89 s were found between groups for use of other diuretics, aspirin, antidepressants, antiepileptics, ant

90 cular disease (CVD) consequences of incident diuretic-associated diabetes compared with the effects o

91 : (1) observational: patients receiving loop diuretics at the Yale Transitional Care Center (N=162) a

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

93 st three antihypertensive drugs, including a diuretic, at the optimum doses.

94 erated doses of at least 3 drugs including a diuretic before randomization.

95 ontrast media, antiinflamatory, cytostatics, diuretics, beta blockers, anesthetics, analgesics, antie

96 Overall, the use of thiazide diuretics, beta-blockers, angiotensin-converting enzyme

97 iabetes, hypertension medications, including diuretics, blood lead levels, and hyperlipidemia, the od

98 cs) to identify novel biomarkers of thiazide diuretics BP response.

99 VASP as a potential determinant of thiazide diuretics BP response.

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

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

102 or inhibition of it with the clinically used diuretic bumetanide potently suppresses ammonia-induced

103 on this mechanism, we propose the use of the diuretic bumetanide to prevent the requirement for BDNF

104 ce NKCC2 is the molecular target of the loop diuretics bumetanide and furosemide, we asked about thei

105 potassium after the initiation of digoxin or diuretics by Medicare beneficiaries.

106 I receptor blockers, beta-blockers, thiazide diuretics, calcium channel blockers, and metformin.

107 nsitive to flow changes in kidney induced by diuretic challenges.

108 ds pharmacologic monotherapy with a thiazide diuretic, citrate, or allopurinol to prevent recurrent n

109 Treatment with an aminoglycoside-diuretic combination produced loss of all outer hair cel

110 Rodents chronically administered loop diuretics develop DR due to compensatory distal tubular

111 Diuretics, developed more than four decades ago, are use

112 nce of comorbidities, and were more often on diuretics, digoxin, and angiotensin converting enzyme in

113 Loop diuretic dose (furosemide equivalent) was 80 (40, 140) m

114 sed significantly, even after correction for diuretic dose (P=0.040 and 0.004, respectively), leading

115 s no longer significant after correction for diuretic dose (P=0.263), indicating preserved diuretic e

116 correlation between DE and both intravenous diuretic dose and net fluid output (r(2)</=0.26 for all

117 Higher diuretic dose was a strong predictor of higher urine out

118 Diuretic dose was a strong predictor of urine output.

119 ment in self-care management (e.g. adjusting diuretic dose) or the ability to act on changes in sympt

120 urvival even after adjusting for in-hospital diuretic dose, fluid output, in addition to baseline cha

121 formation beyond that of raw fluid output or diuretic dose.

122 ciency, fluid output, hemoconcentration, and diuretic dose.

123 oconcentration had higher average daily loop diuretic doses (p = 0.001), greater weight loss (p < 0.0

124 n a positive sodium balance with twice-daily diuretic dosing.

125 that spironolactone (SPIR), an FDA-approved diuretic drug with a long-term safety profile, can up-re

126 petite induced in rats by treatment with the diuretic drug, furosemide.

127 de, consistent with the hypothesis that loop diuretic drugs bind within the translocation cavity.

128 After intravenous administration of a diuretic, dual-phase CT urography was performed at 60 se

129 xidant, nephro- and hepato-protective, renal/diuretic effect, effects on lipid metabolism (anti-chole

130 with bumetanide is compromised by its potent diuretic effect.

131 s, down-regulated in expression, that have a diuretic effect.

132 on mechanisms provides insight into thiazide diuretic efficacy.

133 s a result, we hypothesized that a metric of diuretic efficiency (DE) would capture distinct prognost

134 iuretic dose (P=0.263), indicating preserved diuretic efficiency during the study.

135 sening renal function was not increased, and diuretic efficiency was significantly improved with the

136 amined across a range of parameters, such as diuretic efficiency, fluid output, hemoconcentration, an

137 otassium channel, ROMK, will represent novel diuretics for the treatment of hypertension.

138 ounder of epidemiology studies is the use of diuretics for treating hypertension.

139 Cotreatment with the diuretic furosemide in wild-type mice attenuated rosigli

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

141 UP CT urography after injection of a diuretic has a higher lesion detection rate than the EP

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

143 In this study, we describe a novel role for diuretic hormone 31 (DH31), the fly homolog of the verte

144 y cells in the Drosophila brain that produce Diuretic hormone 44 (Dh44), a homolog of the mammalian c

145 ted by a brain signaling pathway composed of diuretic hormone 44 (Dh44), a neuropeptide related to ve

146 ty are unclear, but involve the neuropeptide diuretic hormone 44 (DH44), an ortholog of corticotropin

147 m, and the neuropeptide leucokinin (LK) is a diuretic hormone that also modulates feeding.

148 ic (HR 1.48 [95% CI 1.11, 1.98]), a thiazide diuretic (HR 1.44 [95% CI 1.00, 2.10]), or a loop diuret

149 Use of any diuretic (HR 1.48 [95% CI 1.11, 1.98]), a thiazide diure

150 tic (HR 1.44 [95% CI 1.00, 2.10]), or a loop diuretic (HR 2.31 [95% CI 1.36, 3.91]) was associated wi

151 On univariable analysis, only diuretics, hsCRP, GZ, and core scar were associated with

152 ect renin inhibitor, aliskiren (n = 7), or a diuretic, hydrochlorothiazide (n = 7), for 6 months.

153 at the addition of tolvaptan to a background diuretic improved dyspnea early in patients selected for

154 had heart failure or hypertension initiating diuretic in 2011 and 8683 beneficiaries who had heart fa

155 ablation of claudin-14 or the use of a loop diuretic in mice abrogated HDAC inhibitor-induced hypoca

156 r, calcium channel blocker, or thiazide-type diuretic in the nonblack hypertensive population, includ

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

158 our study demonstrate increased use of loop diuretics in patients with BP before the development of

159 late osmotic stability are disrupted by loop diuretics in rats.

160 are not understood, including the action of diuretics in the treatment of ascites and the ability of

161 st three antihypertensive drugs, including a diuretic, in adequate doses) and confirmed by 24-h ambul

162 ous antiarrhythmic drug use, previous use of diuretics, increased left atrial diameter, increased lef

163 ed 6-hour urine collections to quantify loop diuretic-induced cumulative sodium output.

164 Overcoming diuretic-induced hyperuricaemia is difficult and there i

165 A closer understanding of the mechanisms of diuretic-induced hyperuricaemia may lead to the creation

166 The mechanism for diuretic-induced hyperuricaemia may operate through volu

167 Thus, pendrin may attenuate diuretic-induced salt loss, but this function remains un

168 uartile range, 15.6%-75.7%) of the estimated diuretic-induced sodium release did not undergo distal r

169 r TM3 residues in ion translocation and loop diuretic inhibition.

170 , a calcium channel blocker or thiazide-type diuretic is recommended as initial therapy.

171 Potassium depletion by thiazide diuretics is associated with a rise in blood glucose.

172 t four, antihypertensive agents (including a diuretic), is associated with higher risk of secondary h

173 mbination, particularly including a thiazide diuretic, is very often necessary and should be started

174 After controlling for urine diuretic levels, the increase in FELi explained only 6.4

175 fit patients with type 2 diabetes who need a diuretic-like effect to optimise control of blood pressu

176 that inexpensive and well-tolerated thiazide diuretics may be especially effective in preventing the

177 in cells expressing NCC, indicating thiazide diuretics may be particularly effective for lowering BP

178 vious concerns about the safety of high-dose diuretics may not be valid.

179 The diuretic mechanism of UT inhibitors may complement the a

180 Patients treated with diuretics (n=4) displayed higher abundance of full-lengt

181 in a control cohort without HF not receiving diuretics (n=52; 16.6%+/-9.2%; P=0.82).

182 rs, beta-blockers, calcium channel blockers, diuretics, nitrates, statins, insulin, biguanides, sulfo

183 incident gout as compared with not using any diuretic, not using a thiazide diuretic, or not using a

184 nd ACEI+BB strictly dominated treatment with diuretics only (cost-saving).

185 ional Institutes of Health HF Network, DOSE (Diuretic Optimization Strategies Evaluation) and ROSE (R

186 However, the recently published DOSE (Diuretic Optimization Strategies Evaluation) trial sugge

187 as performed of 496 patients enrolled in the Diuretic Optimization Strategy Evaluation in Acute Decom

188 e analysis of the randomized clinical trial, diuretic optimization strategy evaluation in acute heart

189 Rather than the absolute dose of diuretic or urine output, the primary signal of interest

190 In Medicare beneficiaries initiating diuretics or digoxin, this study examined disparities in

191 bate cardiovascular problems from overuse of diuretics or inotropes because of the unusual loading co

192 , are usually treated with potassium-sparing diuretics or nonsteroidal anti-inflammatory drugs and or

193 g lung disease, beta-blocker, ACE-inhibitor, diuretic, or antihypertensive medication use in aggregat

194 eart failure on problem list, inpatient loop diuretic, or brain natriuretic peptide level of 500 pg/m

195 not using any diuretic, not using a thiazide diuretic, or not using a loop diuretic, respectively.

196 Loop diuretics other than furosemide were converted to furose

197 t loss (p < 0.001), later transition to oral diuretics (p = 0.03), and shorter length of stay (p < 0.

198 with truly resistant hypertension, thiazide diuretics, particularly chlorthalidone, should be consid

199 correcting for relevant variables (including diuretics, pH, potassium levels and renal sodium excreti

200 Diuretics reduce the rate of action potential fall in th

201 ienopyrimidines may be useful for therapy of diuretic-refractory edema in heart and liver failure.

202 tion of pendrin and NCC can provide a strong diuretic regimen without causing hypokalemia for patient

203 0.7 [95% confidence interval, 0.57-0.82] for diuretics; relative risk, 0.8 [95% confidence interval,

204 eys immediately before and immediately after diuretic renal scintigraphy (reference standard for pres

205 Understanding the tubular location of diuretic resistance (DR) in heart failure (HF) is critic

206 <60 ml/min/1.73 m(2); 2) hyponatremia; or 3) diuretic resistance (urine output </=125 ml/h following

207 renal perfusion and oxygenation, leading to diuretic resistance and recurrent hospitalization.

208 associated with neurohormonal activation and diuretic resistance with chloride depletion as a candida

209 Renal dysfunction, diuretic resistance, and hyponatremia represent treatmen

210 zed by a rise in serum creatinine, oliguria, diuretic resistance, and in many cases, worsening of ADH

211 high doses may relieve congestion, overcome diuretic resistance, and mitigate the effects of adverse

212 is balanced by the recognized limitations of diuretic resistance, neurohormonal activation, and worse

213 ongestive heart failure, nephrotic syndrome, diuretic resistance, or generalized edema.

214 l a complex mechanism that explains thiazide diuretic resistance.

215 of hypertension and edema, perhaps including diuretic-resistant edema.

216 ing a thiazide diuretic, or not using a loop diuretic, respectively.

217 Diuretic response (defined as weight change per 40 mg of

218 Hypochloremia was associated with poor diuretic response (odds ratio, 7.3; 95% confidence inter

219 Both diuretic response and hemoconcentration are indicators o

220 o 0.82; P=0.004) for patients with favorable diuretic response and hemoconcentration compared with al

221 Patients who displayed both favorable diuretic response and hemoconcentration had a markedly l

222 This study examines the value of combining diuretic response and hemoconcentration to better predic

223 e tools for rapid and accurate prediction of diuretic response are needed.

224 ators of decongestion, hemoconcentration and diuretic response improves risk prediction for early reh

225 The postingestion diuretic response is likely to be influenced by several

226 Poor diuretic response was associated with low systolic blood

227 arterial pressure and determine the initial diuretic response, but septic acute kidney injury develo

228 e was associated with high bicarbonate, poor diuretic response, less hemoconcentration, and worsening

229 e primary signal of interest when evaluating diuretic responsiveness is the efficiency with which the

230 he hospitalization should similarly identify diuretic responsiveness, but hemoconcentration this earl

231 ion between (changes in) chloride levels and diuretic responsiveness, decongestion, and mortality in

232 inition that excluded the intensification of diuretics resulted in a lower event rate but a stronger

233 pressin receptor antagonists, urea, and loop diuretics serve this purpose, but received different rec

234 ntihypertensive drug regimens that include a diuretic, should be complemented by the sequential addit

235 The diuretics spironolactone and trichlormethiazide, but not

236 unds (mixture of anabolics, beta-2 agonists, diuretics, stimulants, narcotics, and beta-blockers) spi

237 imary urine production and responsiveness to diuretic stimuli.

238 ese proteins could have therapeutic use as a diuretic strategy.

239 50% after intravenous administration of the diuretic (T1/2).

240 omise as a renal proximal tubule natriuretic/diuretic target for the treatment of fluid-retaining sta

241 inward rectifier potassium (Kir) channel and diuretic target, Kir1.1.

242 harmacological validation of ROMK as a novel diuretic target.

243 n developing new classes of antihypertensive diuretics targeting ROMK.

244 was confirmed by the natriuretic response to diuretics targeting the thick ascending limb, the distal

245 neurohormonal activation, and regulation of diuretic targets, and hypochloremia predicts mortality i

246 Thiazide diuretics (TD) are commonly prescribed anti-hypertensive

247 BUM5, but not BUM1, was less diuretic than bumetanide, so that BUM5 was further evalu

248 ASIC1 through amiloride, a potassium sparing diuretic that is currently licensed for hypertension and

249 n may allow for less intensification of loop diuretic therapy and a lower incidence of worsening rena

250 ia, or an inadequate response to traditional diuretic therapy despite dose escalation.

251 ltrafiltration is an alternative strategy to diuretic therapy for the treatment of patients with acut

252 hour intervals, in addition to combinational diuretic therapy in approximately 70% and both oral spir

253 Symptomatic improvement with diuretic therapy supports the presence of HFpEF in patie

254 nd chloride excretion, creatinine clearance, diuretic therapy, pH, known diabetes and intensive care

255 f metrics of renal function and preadmission diuretic therapy, traditional baseline characteristics,

256 potential utility of pendrin inhibitors for diuretic therapy, we tested in mice a small-molecule pen

257 atrial fibrillation, pacemakers, and chronic diuretic therapy.

258 ht provide insightful information to titrate diuretic therapy.

259 ion or improved renal function when added to diuretic therapy.

260 f changes observed following paracentesis or diuretic therapy.

261 dical management with heart rate control and diuretic therapy.

262 uggest that administration of high-dose loop diuretics to patients with HF yields meaningful increase

263 in converting enzyme (ACE) inhibitor or loop diuretics to those 75 years or older without assessment

264 Thiazide diuretics treat the disease, fostering the view that hyp

265 c patients indicate that citrate or thiazide diuretic treatment may improve BMD.

266 out and hyperuricaemia with hypertension and diuretic treatment.

267 Five patients underwent follow-up MR after diuretic treatment.

268 argets for development of drugs with a novel diuretic ('urearetic') mechanism.

269 D deficiency (OR, 1.14; 95% CI, 1.05-1.22), diuretic use (OR, 1.13; 95% CI, 1.07-1.18), and renal in

270 .239; 95% CI, 0.140-0.408), and preoperative diuretic use (RYGB: OR, 1.729; 95% CI, 1.462-2.045 and A

271 espectively; P = .008), as well as increased diuretic use and pulmonary edema on first chest x-ray, w

272 95% CI, 7.9-10.6]; P<0.001), a lower risk of diuretic use at discharge (odds ratio, 0.4; 95% CI, 0.25

273 was 5.57+/-1.48 mg/dL; male sex, higher BMI, diuretic use, and lower GFR were associated with higher

274 obesity status, purine intake, alcohol use, diuretic use, and use of antigout medications.

275 ng status, alcohol use, daily blocks walked, diuretic use, estimated glomerular filtration rate, left

276 a at rest or with mild exertion, intravenous diuretic use, glomerular filtration rate of 30 to 75 mL/

277 ter adjustment for renal function, diabetes, diuretic use, hypertension, race, body mass index, incom

278 multivariate analysis included pre-operative diuretic use, longer cardiopulmonary bypass time, operat

279 The prevalence of atrial fibrillation and diuretic use, n-terminal probrain natriuretic peptide le

280 line use and of squamous cell carcinoma with diuretic use.

281 od pressure less than 140/90 mm Hg; thiazide diuretics used in multidrug hypertensive regimen; athero

282 reduction in office SBP produced by the two diuretics was identical, further strengthening the case

283 enal function (p = 0.01), whereas total dose diuretics was lower in patients with hemoconcentration (

284 ding intravenous treatment with inotropes or diuretics was the most common adverse event (in 20 [2%]

285 or other antihypertensive therapy (excluding diuretics) was administered at year 1.

286 or other antihypertensive therapy (excluding diuretics) was administered at year 1.

287 The resulting natriuresis-driven diuretic water loss is assumed to control the extracellu

288 Thiazide and loop diuretics were associated with higher risk of incident g

289 nd scheduled treatment with intravenous loop diuretics were included.

290 Beneficiaries initiating diuretics were less likely to have testing if they were

291 , calcium channel blockers were inferior and diuretics were superior to other drug classes.

292 Loop diuretics were used significantly more frequently by the

293 Disease features are reversed by thiazide diuretics, which inhibit the Na-Cl cotransporter in the

294 rs may complement the action of conventional diuretics, which target sodium transport.

295 ept for NSAIDs, ACE inhibitors, and thiazide diuretics, which were more prevalent in black patients.

296 re likely to be treated with higher doses of diuretics, while higher filling pressures, N-terminal pr

297 Beneficiaries initiating diuretics with laboratory values were more likely to hav

298 bitors are first in their class salt-sparing diuretics with potential clinical indications in volume-

299 r more effective fluid removal compared with diuretics, with improved quality of life and reduced reh

300 ive management includes salt restriction and diuretics, with thoracentesis and transjugular intrahepa

301 .73, 0.58-0.91); or an ACE inhibitor or loop diuretic without appropriate monitoring (0.51, 0.34-0.78

302 study treatment in the following subgroups: diuretics (yes/no), digitalis glycoside (yes/no), minera