Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DIURETICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMed1984

Diuretics, potassium depletion and the risk of arrhythmias.

Evidence is available which suggests that the use of thiazide diuretics in the treatment of essential hypertension causes a fall in both plasma and total body potassium. The incidence of ventricular arrhythmias is proportional to the potassium deficit and may be enhanced by concomitant magnesium deficiency. Potassium loss may be minimized by limiting the dose of diuretic and by restricting sodium intake. Potassium chloride supplements are of relatively limited value and potassium-conserving diuretics are to be preferred in aviators. To reduce the potential risk of rhythm disturbance, aircrew receiving thiazide diuretics should be managed to ensure a serum potassium level at least 3.5 mmol l-1 after stabilization on therapy.

Aerospace Medicine↗
PubMed1999

Rapid screening for diuretic doping agents in urine by C60-assisted laser-desorption-ionization-time-of-flight mass spectrometry.

This study describes a matrix-assisted laser-desorption-ionization (MALDI) mass spectrometry for rapid screening of 12 diuretics in spiked urine. C60 is used as the matrix for MALDI. Diuretics are directly analyzed by C60-MALDI without previous derivatization. The fact that most diuretic molecules contain sulfate groups accounts for why anions of the molecules can be easily desorbed and ionized in MALDI. Using C60 as the matrix is advantageous because of the low background in the low mass range on the negative MALDI mass spectrum. A clear mass window between m/z 200 and 600 in negative ion mode is also obtained. Only a minimum amount of the sample (< 1 microL) is necessary to perform the analysis. The detection limit of diuretics is approximately 0.1-1 microg/mL.

Benzothiadiazines↗
PubMed1997

Loop diuretics in the management of acute renal failure: a prospective, double-blind, placebo-controlled, randomized study.

BACKGROUND: Studies on the role of loop diuretics in patients with acute renal failure (ARF) are largely retrospective, anecdotal, and poorly controlled. We report the results of a prospective, randomized, placebo-controlled, double-blind study examining the effect of loop diuretics on renal recovery, dialysis, and death in patients with ARF. METHODS: Ninety-two patients with ARF were enrolled into the study. All received intravenous dopamine, 2 micrograms/kg body weight/min throughout, 20% mannitol, 100 ml every 6 h for the first 3 days, and, in a double-blind manner, either torasemide, frusemide, or placebo, 3 mg/kg body weight i.v. every 6 h for 21 days or until renal recovery or death. RESULTS: Renal recovery, the need for dialysis, and death were no different in the three groups. Patients given a loop diuretic had a significant rise in urine flow rate in the first 24 h compared to placebo (P = 0.02). Based on the urine flow rate during the first post-medication day patients were divided into two groups--oliguric (< 50 ml/h) and non-oliguric (> or = 50 ml/h). Non-oliguric patients had a significantly lower mortality than oliguric patients (43% vs 69%, P = 0.01). However, they were less ill (APACHE II score 17.2 vs 20.6, P = 0.008) and had less severe renal failure at entry (creatinine clearance 14 ml/min vs 4 ml/min, P < 0.0001). CONCLUSION: The use of loop diuretics in oliguric patients with ARF can result in a diuresis. There is no evidence that these drugs can alter outcome.

Acute Kidney Injury↗
PubMed1997

Hypertension, diuretics, and antihypertensive medications as possible risk factors for renal cell cancer.

The authors examined the relation of hypertension, use of diuretics, and use of antihypertensive medications to the risk of fatal renal cell cancer in a prospective cohort study of 998,904 adult Americans followed for 7 years (1982-1989). Analysis included 335 renal cell cancer deaths (123 in women and 212 in men). Cox proportional hazards modeling was used to calculate rate ratios. Increased rate ratios were present for cigarette smoking in men and for elevated body mass index in both sexes. Significantly increased age-matched rate ratios, independent of smoking and body mass index, were present for hypertension, use of diuretics, and use of hypertension medications, but only for women. Multivariate testing confined these risks to hypertensive women who were using hypertension medications alone (rate ratio = 2.2, 95% confidence interval 1.4-3.5) or with diuretics (rate ratio 2.5, 95% confidence interval 1.5-4.3). Risk was not significantly increased for either men or women who had untreated hypertension or who used diuretics alone with or without hypertension. These findings partly support those of earlier studies suggesting that medications related to treatment of hypertension, or the severity of hypertension itself, may contribute to the etiology of renal cell cancer.

Adult↗
PubMed1990

Potential benefit of combination therapy with diuretics and beta blockers having intrinsic sympathomimetic activity.

When combining a beta blocker with a diuretic in patients with hypertension, consideration should be given to the potential advantages of intrinsic sympathomimetic activity (ISA). During long-term administration of a beta blocker without ISA, total peripheral resistance stabilizes at or slightly above the pretreatment level. Since cardiac output is decreased, blood pressure falls. Thus, beta blockers without ISA may exacerbate the underlying haemodynamic abnormality of long-standing hypertension, increased systemic resistance. In contrast, the reduction in pressure which occurs with a beta blocker possessing a high degree of ISA, such as pindolol, is associated with a reduction in total peripheral resistance and little change in cardiac output. Thiazide diuretics and most beta blockers without ISA also have an adverse impact on the blood lipid profile, potentially increasing cardiovascular risk. With the exception of oxprenolol, monotherapy with beta blockers which possess ISA have generally had no adverse blood lipid changes. Indeed, pindolol has been shown to increase HDL-cholesterol and to reduce the ratio of total cholesterol to HDL-cholesterol. Pindolol administered in combination with several diuretics has not increased the adverse lipid effects of these agents and, in some studies, evidence suggests that pindolol may counteract some or all of these changes. The clinical significance of these differences between beta blockers with and without ISA remains uncertain. Nevertheless, the potential haemodynamic and metabolic benefit of agents with ISA mandate that they receive careful consideration when selecting a beta blocker to administer with a diuretic.

Adrenergic beta-Antagonists↗
PubMed2004

Severe hyponatremia associated with the combined use of thiazide diuretics and selective serotonin reuptake inhibitors.

Thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs) are among the most commonly prescribed medications. Each medication has been associated with the development of severe hyponatremia. The mechanisms involved in the development of hyponatremia differ for each medication. Thiazide diuretics induce hyponatremia by impairment of urinary dilution, renal loss of sodium and potassium, stimulation of antidiuretic hormone (ADH), and perhaps from a dipsogenic effect. SSRIs cause hyponatremia through the syndrome of inappropriate ADH release. Two cases of severe hyponatremia in patients taking both a thiazide diuretic and an SSRI highlight the possibility of a synergistic effect in impairment of renal free water clearance when both medications are given. These two cases serve as a cautionary example and should prompt careful monitoring of patients prescribed both an SSRI and a thiazide diuretic (especially in elderly women, who seem to be at increased risk for this complication).

Aged↗
PubMed1997

Protocol-guided diuretic management: comparison of furosemide by continuous infusion and intermittent bolus.

OBJECTIVE: To evaluate the safety and relative effectiveness of two diuretic protocols in the intensive care unit (ICU). DESIGN: Prospective, randomized comparative study. PATIENTS: Thirty-three cardiac and medical ICU patients with pulmonary edema or fluid overload for which aggressive diuresis was intended. INTERVENTIONS: Enrolled patients were randomized to fluid management strategies combining fluid restriction and individually adjusted diuretic therapy by either continuous or bolus infusions of furosemide, titrated to achieve negative hourly fluid balance. MEASUREMENTS AND MAIN RESULTS: Cumulative intake minus output (primary endpoint); change in serum creatinine, and length of ICU and hospital stay (secondary endpoints). Diuresis by either protocol was feasible, safe, and effective. The main outcome measures were not significantly different for either group managed with a standardized protocol. CONCLUSIONS: Protocol-guided diuretic management, with individualized titration of dosage to defined physiologic endpoints can be readily and safely implemented in the ICU. Both continuous and bolus diuretic regimens appear equally effective in achieving negative fluid balance. Larger studies with a randomized control arm are needed before these protocols can be recommended as routine practice.

APACHE↗
PubMed1990

The cardiotoxicity of thiazide diuretics: review of the evidence.

Careful consideration of all relevant scientific evidence and a critical assessment of data quality show that thiazide diuretics are not cardiotoxic. Of 12 reported trials only two recorded more coronary heart disease events in thiazide-treated patients than in controls. One of these two was a subgroup of a larger study (Heart Attack Prevention in Primary Hypertension, HAPPHY) which found no difference between thiazide-treated and beta-blocker-treated patients. The other, the Oslo study, was too small to allow valid conclusions. Results from a subgroup in the Multiple Risk Factor Intervention Trial (MRFIT) that appeared to supply evidence for thiazide-related cardiotoxicity are suspect when examined critically. Further evidence from 24- to 28-h ECG monitoring does not support the hypothesis that thiazide diuretics, either in the presence or absence of hypokalemia, increase the frequency or severity of ventricular arrhythmias. Reports of a thiazide-induced intracellular magnesium deficiency as a cause of ventricular arrhythmias have also not been confirmed; the development of arrhythmias in acute myocardial infarction appears to be due to an increase in catecholamine levels rather than hypokalemia. There appears to be little evidence to support the assumption that long-term use of thiazide diuretics aggravates or accelerates atherosclerosis of the coronary arteries; any fall in serum cholesterol appears to be transient. For the great majority of patients with uncomplicated hypertension, without a previous myocardial infarction, congestive heart failure, diabetes mellitus or gout, thiazide diuretics appear to be both safe and effective antihypertensive agents.

Arrhythmias, Cardiac↗
PubMed2001

Characterization of the antihypertensive effect of a thiazide diuretic in angiotensin II-induced hypertension.

OBJECTIVES: The antihypertensive effect of thiazide diuretics in angiotensin II induced hypertension has never been characterized. In the current study, we sought to determine the effect of a thiazide diuretic on arterial pressure and renal fluid excretion in rats receiving a chronic intravenous infusion of angiotensin II while on fixed normal or high sodium intakes. DESIGN AND METHODS: Male rats were chronically instrumented with arterial and venous catheters for drug injection and direct daily measurements of blood pressure and heart rate. Rats were maintained on high salt intake (HS), 6 mEq/day, or on normal salt intake (NS), 2 mEq/day. Rats were randomly assigned to four groups: HS and NS with 15 day angiotensin II infusion (5 ng/min) and HS and NS without angiotensin II infusion. Trichlormethiazide (TCM), a thiazide diuretic, was orally administered, approximately 10 mg/kg per day, for the middle 5 days of angiotensin II infusion. RESULTS: Only HS rats receiving angiotensin II infusion became hypertensive. Angiotensin II infusion did not produce changes in heart rate, sodium balance or water balance. Chronic administration of TCM significantly reduced mean arterial pressure (MAP) within 24 h in HS rats receiving angiotensin II, but did not affect MAP in any other group. TCM produced a similar loss of Na+ and water in all rats. Blood volumes and plasma electrolytes did not change during the study. CONCLUSIONS: The antihypertensive effects of thiazide diuretics are not due exclusively to volume depletion. We propose that salt and water loss caused by TCM may lower MAP by impairment of salt-sensitive pressor mechanisms activated by angiotensin II.

Angiotensin II↗
PubMedDate not supplied

Antihypertensive effects of captopril in combination with diuretics in spontaneously hypertensive rats.

To examine the antihypertensive effects of captopril, when used in combination with diuretics, an oral dose of the agent (30 mg/kg) was given to spontaneously hypertensive rats pretreated for 1 week with trichlormethiazide (TCTZ), hydrochlorothiazide (HCTZ), furosemide, or water. One-week treatment with diuretics did not lower blood pressure, but potentiated the anti-hypertensive action of captopril in magnitude as well as duration. The degree of potentiation was in the following order: furosemide greater than or equal to HCTZ greater than TCTZ. Plasma renin concentration (PRC) prior to the administration of captopril was highest in the furosemide group, followed by the HCTZ, TCTZ, and control groups, in this order. When data from four groups were taken together, the reduction of blood pressure following captopril administration was closely related to PRC before administration. These data suggest that repeated administration of diuretics renders the maintenance of blood pressure more dependent on the renin-angiotensin system without affecting blood pressure and that this situation underlies the potentiation of the antihypertensive action of captopril by combined use of diuretics. There was no qualitative difference between furosemide and thiazides in the potentiation of anti-hypertensive action of captopril.

Aldosterone↗
PubMed1984

Diuretics, sodium intake, and renin in the management of hypertension.

Twenty-four-hour urinary sodium excretion and plasma renin activity were monitored in 36 patients receiving bendrofluazide as sole antihypertensive therapy. There was no increase in urinary sodium output compared with pretreatment values during a 2-year period, and there is therefore no evidence that an increase in salt appetite as a result of salt depletion occurred. However, plasma renin activity progressively increased over a 2-year period. In five of eight patients who initially had a subnormal renin response to the diuretic, plasma renin level rose into the normal stimulated range. When administration of the diuretic was stopped in 10 patients after a mean treatment period of 49 months, plasma renin activity promptly fell and weight increased significantly, although blood pressure did not rise. However, on rechallenging with bendrofluazide 28 days later, a greater response was observed than when treatment was originally instituted. Further, three of five patients with low renin hypertension had a normal response on the second occasion. Thus prolonged diuretic therapy has a persistent effect on the activity of the renin-angiotensin system as well as on blood pressure for at least 4 weeks after the discontinuation of diuretics.

Adult↗
PubMed1985

Antihypertensive treatment using calcium antagonists in combination with captopril rather than diuretics.

The antihypertensive efficacy of combination therapy with the angiotensin-converting enzyme inhibitor captopril and a diuretic or a calcium antagonist was compared in 16 patients with essential hypertension with a blood pressure of over 160/95 mm Hg having triple drug therapy. While monotherapy with a calcium antagonist--usually verapamil 500 mg/day or nitrendipine 70 mg/day--did not reduce diastolic blood pressure to greater than 95 mm Hg, this goal was achieved in 15 out of 16 patients with the combination of captopril (53 mg/day) and the calcium antagonists in the above dose (151 +/- 4/88 +/- 2 SEM mm Hg) and in 13 out of 16 patients with captopril (84 mg/day) and a diuretic (158 +/- 4/91 +/- 1 mm Hg). There was a direct relationship between intraindividual pressure responses to the two drug combinations (r = 0.88, p less than 0.001). Heart rate was similar and weight lower on the captopril-diuretic combination. Captopril's antihypertensive efficacy can be equally enhanced by calcium antagonists (without affecting renin long term) as by diuretics, which are thought to work by stimulating the renin-angiotensin system. The calcium antagonist-captopril combination may be of particular advantage in hypertensive patients who are otherwise difficult to treat.

Adult↗
PubMed1989

Angiotensin converting enzyme inhibitors enhance the antihypertensive efficacy of diuretics and blunt or prevent adverse metabolic effects.

Angiotensin converting enzyme (ACE) inhibition has provided a new approach to the treatment of hypertension. The broad efficacy of ACE inhibitors across the entire spectrum of hypertension exceeds original predictions. Diuretics have been shown to extend efficacy to over 85% of noncomplicated hypertensives. In addition to efficacy, combination of ACE inhibitors with diuretics permits prevention or attenuation of many undesirable side effects of diuretic therapy, including hypokalemia, hyperuricemia, hyperglycemia, and hypercholesterolemia. Thus, considerations of both efficacy and beneficial effects on cardiovascular disease risk factors make the combination of ACE inhibitors and diuretics an attractive one in the treatment of hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Loop diuretic therapy in liver cirrhosis with ascites.

Medical treatment of ascites is aimed at reverting sodium retention, that is, at creating a negative sodium balance to relieve ascites. Bed rest and low-sodium diet induce the disappearance of ascites in about 10% of patients. Loop diuretics and aldosterone antagonists must be administered to the patients not responding to the previous regimen. Available evidence indicates that aldosterone antagonists are the first-choice drugs, as these substances are more effective than furosemide. Nevertheless, loop diuretics potentiate the effects of aldosterone antagonists. The reduced efficacy of furosemide in these patients, when compared with that of spironolactone, may be related to an impairment of both pharmacodynamics and pharmacokinetics. In fact, most sodium not reabsorbed in Henle's loop, due to the action of furosemide, is subsequently taken up in the distal nephron because of hyperaldosteronism. A further mechanism of resistance may be related to an impaired excretion of furosemide into the tubular lumen. The use of diuretics in the treatment of ascites is associated with several side effects, including prerenal azotemia, hepatic encephalopathy, and electrolyte and acid-base disorders. A stepped-care approach, together with careful monitoring of patients, is the best way to reduce the incidence of these complications. Ethacrynic acid has been shown to be highly effective in the treatment of ascites, even in patients refractory to other diuretics, but its use is associated with a high incidence of hypokalemia and hypochloremic alkalosis. Bumetanide and piretanide are comparable to furosemide, in terms of both efficacy and side effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Ascites↗
PubMed2001

Comparison of neurohumoral effects of short-acting and long-acting loop diuretics in patients with chronic congestive heart failure.

We evaluated the comparative effects of furosemide, a short-acting loop diuretic, and azosemide, a long-acting loop diuretic, on neurohumoral factors and quality of life (QOL) in patients with congestive heart failure (CHF). Twenty-five stable patients with mild chronic CHF who had been administered furosemide (n = 14) or azosemide (n = 11) orally for more than 3 months were studied. We changed furosemide to azosemide or azosemide to furosemide and followed for 3 months. Echocardiography was performed, and we also measured neurohumoral factors and assessed QOL by questionnaire. Blood pressure, body weight, renal function and echocardiographic findings were the same during the furosemide and azosemide treatments. Plasma levels of atrial natriuretic peptide and brain natriuretic peptide were not different between the two treatments. However, plasma concentrations of active renin and norepinephrine were significantly higher with furosemide treatment than with azosemide treatment. QOL score was significantly lower with azosemide than with furosemide. These findings suggest that long-acting loop diuretics may have fewer adverse effects on the neuroendocrine system and QOL than short-acting loop diuretics in patients with mild CHF.

Administration, Oral↗
PubMed2003

99mTc-MAG3 diuretic renography in children: a comparison between F0 and F+20.

The aim of this work was to compare the quality of renal drainage obtained with two well-described procedures of diuretic renography (F+20 and F0 tests). We selected 36 clinically stable children, aged 10 days to 17 years, with unilateral (25) or bilateral (11) hydronephrosis, in whom both F+20 and F0 tests were successively performed. In all cases, a late image (PM) was acquired after micturition and after changing the position of the patient. The following parameters were calculated: the time to the maximum of the basic renogram (Tmax); and the normalized residual activity (NORA) and output efficiency (OE) at the end of the 20 min renogram, at the end of the furosemide test (35 min) and on the PM image. In F+20, the renal drainage was better on the PM image than at the end of the diuretic renogram, whereas, in F0, the renal drainage was better on the PM image than at the end of the 20 min diuretic renogram. When comparing F0 and F+20, both OE and NORA parameters revealed slightly better drainage at the end of the 20 min F0 renogram than at the end of the 35 min F+20 diuretic renogram. The drainage obtained on the late post-voiding image was comparable for both F0 and F+20 tests. In conclusion, the quality of drainage obtained during the F+20 and F0 procedures can easily be compared using both OE and NORA. A very similar quality of drainage was reached for both procedures when considering only the PM image. This PM view remains mandatory irrespective of the timing of the furosemide injection and despite the use of tracers with a high extraction rate.

Adolescent↗
PubMed1995

Effect of diuretic drugs on creatinine clearance determination.

Diuretic drugs have been reported to alter the glomerular filtration rate and possibly the creatinine excretion by the kidneys. We evaluated the effects of single doses of diuretic drugs on creatinine clearance determination. Ten healthy volunteers were randomized to receive either oral hydrochlorothiazide, oral furosemide, intravenous furosemide, or no treatment in a cross-over fashion during four separate test days with 6-day washout periods. Urine and blood specimens were collected during 24 h after the treatments. Specimens were assayed for creatinine, and the creatinine clearance corresponding to the 4-, 6-, 12-, and 24-h urine collections were calculated. Analysis of variance did not show a statistically significant effect of the diuretic regimens on creatinine clearance over these periods. This study demonstrates that single doses of diuretic drugs do not have significant effect on creatinine clearance determination using urine collected during 4-24-h periods.

Administration, Oral↗
PubMed1980

Studies on the mechanism and characteristics of action of a uricosuric diuretic, indacrinone (MK-196).

1 The renal action of indacrinone (MK-196), a phenoxyacetic acid derivative with diuretic and uricosuric properties, has been studied in fifteen male subjects. 2 Increasing single doses of up to 60 mg of oral indacrinone produced a linear increase in urinary volume and excretion of Na+ and Cl-, whilst the responses of urinary K+, Ca2+, Mg2+ and uric acid excretion, rose to a plateau at the 40 mg dose. 3 Indacrinone evoked a rapid diuretic response which reached a maximum of 2-4 h and was largely complete at 8-12 h after administration. 4 During maximal hydration, indacrinone produced a substantial fall in fractional free water clearance (CH2O), from 8.89% to 5.83% of the filtered load of water, associated with an increase in osmolal clearance, from 1.38% to 5.78% of the filtered load of solute. The reduction in CH2O was of the same order as that produced by a dose of ethacrynic acid with comparable saluretic activity and significantly greater than that produced by an equi-saluretic dose of hydrochlorothiazide. These findings imply an action of indacrinone upon solute transport in the diluting segments of the distal tubule. 5 At the time of maximal indacrinone-induced saluresis, which amounted to an increase from 0.48% to 4.61% of the filtered load of NaCl, fractional urate clearance increased from 5.16% to 12.24% of the filtered load of uric acid. 6 Indacrinone is a long acting diuretic, sharing some properties in common with both loop diuretics and benzothiadiazines. The results are discussed in relation to structure-activity amongst derivatives of phenoxyacetic acid.

Diuresis↗