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PubMed2026

Efficacy and safety of human albumin combined with furosemide in acute decompensated heart failure with hepatic dysfunction.

BACKGROUND: Congestion is the most common clinical presentation on admission of patients with acute decompensated heart failure (ADHF). Finding effective ways to alleviate congestion has become a pivotal management step. This study sought to investigate the efficacy and safety of intravenous (IV) albumin use in conjunction with furosemide in patients hospitalized for ADHF with hepatic dysfunction in terms of subjective regression of congestion symptoms and worsening renal function. METHODS: This prospective, open-label, randomized-pragmatic trial recruited 241 patients with hepatic dysfunction hospitalized for ADHF. Patients (78 years, 54% female) were assigned to receive IV albumin with furosemide or IV furosemide alone. The coprimary study endpoints were patients' global assessment of symptoms score, quantified as the area under the curve (AUC) of the score on a visual analog scale, and the change in creatinine levels over 72 hours from admission. RESULTS: The experimental treatment group demonstrated a greater improvement in patients' global assessment of symptoms scores (AUCbaseline-72 h 3,767 vs 3,457 points; P < .001) and a milder increase in creatinine levels (0.07 vs 0.18 mg/dL; P = .045) than the IV furosemide group. The length of stay was 1 day shorter (4 vs 5 days; P < .001) and the incidence of worsening renal function was lower (25% vs 38%; P = .037) in the experimental treatment group. CONCLUSIONS: In this hypothesis generating study, among patients with ADHF and hepatic dysfunction, concomitant use of IV albumin and furosemide for the first 72 hours resulted in a significant improvement in subjective perception symptoms of decongestion and a milder increase in creatinine levels than IV furosemide alone.

Aged↗
PubMed2004

Presumed "sulfa allergy" in patients with intracranial hypertension treated with acetazolamide or furosemide: cross-reactivity, myth or reality?

PURPOSE: To determine whether acetazolamide or furosemide produce allergic cross-reactions in patients with self-reported "sulfa allergy." DESIGN: Retrospective case series. METHODS: A retrospective review included patients with intracranial hypertension and a self-reported sulfa allergy treated with either acetazolamide or furosemide seen at the University of Iowa Hospitals and Clinics from 1972 to 2003. All presumed medication-related side effects were collected, including both predictable adverse effects (for example, paresthesias, fatigue) and unpredictable adverse reactions (for example, cutaneous fixed eruptions, urticaria, Stevens-Johnson syndrome, toxic epidermal necrolysis, angioedema, anaphylaxis). RESULTS: We reviewed 363 charts. Of these, 329 patients (91%) were excluded. Of the remaining 34 cases that did report a so-called sulfa allergy, 13 (38%) received acetazolamide alone, 7 (21%) received furosemide alone, and 14 (41%) received both acetazolamide and furosemide. Of the 27 patients who received acetazolamide, 10 (37%) had no documented allergic cross-reaction to sulfa, and 2 (7%) cases had urticaria. The remaining 15 (56%) of acetazolamide-treated patients experienced predictable adverse reactions for this drug (for example, paresthesias). No patient experienced a severe allergic cross-reaction to sulfa. Of 21 patients who received furosemide, no unpredictable adverse reactions or allergic cross-reactions to sulfa were noted. CONCLUSIONS: We find little clinical or pharmacological evidence to suggest that a self-reported sulfa allergy is likely to produce a life-threatening cross-reaction with acetazolamide or furosemide. These medications should be considered for intracranial hypertension if the risk-to-benefit ratio warrants their use.

Acetazolamide↗
PubMed2006

Effect of inhaled furosemide on air hunger induced in healthy humans.

Recent evidence suggests that inhaled furosemide relieves dyspnoea in patients and in normal subjects made dyspnoeic by external resistive loads combined with added dead-space. Furosemide sensitizes lung inflation receptors in rats, and lung inflation reduces air hunger in humans. We therefore hypothesised that inhaled furosemide acts on the air hunger component of dyspnoea. Ten subjects inhaled aerosolized furosemide (40 mg) or placebo in randomised, double blind, crossover experiments. Air hunger was induced by hypercapnia (50+/-2 mmHg) during constrained ventilation (8+/-0.9 L/min) before and after treatment, and rated by subjects using a 100 mm visual analogue scale. Subjects described a sensation of air hunger with little or no work/effort of breathing. Hypercapnia generated less air hunger in the first trial at 23+/-3 min after start of furosemide treatment (58+/-11% to 39+/-14% full scale); the effect varied substantially among subjects. The mean treatment effect, accounting for placebo, was 13% of full scale (P=0.052). We conclude that 40 mg of inhaled furosemide partially relieves air hunger within 1h and is accompanied by substantial diuresis.

Administration, Inhalation↗
PubMed1993

Hemodynamic and fluid responses to furosemide infusion in the ovine fetus.

OBJECTIVES: The direct effects of furosemide infusion have not been systematically examined in the fetus. Our objective was to explore the hemodynamic and urinary responses to a 4-hour infusion of furosemide into fetal sheep. STUDY DESIGN: Furosemide (0, 1, 5, or 10 mg/hr) was infused into the fetal inferior vena cava for 4 hours in 15 chronically catheterized near-term sheep. RESULTS: Relative to vehicle infusion, furosemide produced dose-dependent increases in fetal arterial pressure (analysis of variance, p < 0.05 when comparing groups), fetal heart rate (p < 0.0001), urine flow (p < 0.0001), and urine osmolality, sodium, and chloride, concentrations (p < 0.0001). Concomitantly, there were dose-dependent decreases in fetoplacental blood volume, fetal plasma chloride (p < 0.0001) and fetal venous pressure (p < 0.05). The changes in urine flow rate and fetal arterial pressure were positively correlated (r = 0.46, p < 0.01), suggesting that the diuresis was mediated in part by fetal arterial pressure. The four-quadrant amniotic fluid index increased during the furosemide infusions but not during vehicle infusions (p = 0.022). CONCLUSIONS: Furosemide infusion caused a marked dose-dependent diuresis in the ovine fetus that appears to be partly mediated by increases in vascular pressure. Although amniotic fluid volume increases and fetal blood volume decreases, the reduction in blood volume was small compared with the urine volume excreted.

Amniotic Fluid↗
PubMed1993

Acute effects of ethanol and ethanol plus furosemide on pancreatic capillary blood flow in rats.

The effects of intravenous ethanol and ethanol plus furosemide on pancreatic capillary blood flow (PCBF) were investigated using a laser-Doppler flowmeter. Forty Sprague-Dawley male rats were divided into 4 groups: (1) control, (2) 80% ethanol, (3) 80% ethanol plus furosemide, and (4) furosemide. Mean arterial blood pressure and heart rate were monitored. Levels of serum amylase, calcium, electrolytes, ethanol, and furosemide (groups 3 and 4) were measured, and samples of pancreatic tissue were obtained. The ethanol and furosemide levels were statistically different (p < 0.05). PCBF significantly decreased (p < 0.05) in group 2, increased (p < 0.05) in group 3, and did not differ (p > 0.05) between groups 1 and 4. Histopathologic analysis revealed swollen acini in group 2 and sparse focal necrosis without acinar swelling in group 3. The depressant effect of ethanol on PCBF may be the result of its direct action on pancreatic cells causing edema and capillary compression rather than on primary vascular control mechanisms that adjust blood flow. Furosemide counters this effect.

Amylases↗
PubMed1997

Addition of a thiazide: an effective remedy for furosemide resistance after cardiac operations.

BACKGROUND: The frequent use of diuretic drugs in cardiac surgical practice contrasts with the lack of documentation regarding diuretic treatment in this setting. The aims of this study were to delineate the need for diuretic drugs in adult cardiac surgical practice and to evaluate the impact of adding a combination of 50 mg hydrochlorothiazide and 5 mg amiloride orally to patients responding poorly to furosemide. METHODS: Two hundred ten consecutive patients, 159 undergoing coronary artery bypass grafting procedures and 51 having valve operations, were studied. RESULTS: Seventy-seven patients received large doses of furosemide (> or = 80 mg/24 h) at some time during the postoperative course, and of these 20 responded poorly to furosemide (weight loss 0.3 +/- 0.2 kg) despite considerable fluid retention. The addition of hydrochlorothiazide and amiloride provided a prompt and effective remedy to relative furosemide resistance. Average weight loss was 2.3 +/- 0.2 kg (p < 0.01 compared with response to furosemide) and average diuresis was 2,949 +/- 156 mL in the following 24 hours. CONCLUSIONS: Relative furosemide resistance is common after cardiac operations. Thiazides, although they are mild diuretic agents, may serve as useful adjuncts in this setting.

Administration, Oral↗
PubMed2001

Effects of furosemide on the tubular reabsorption of nitrates in anesthetized dogs.

The present study was performed to determine the tubular sites of nitrite and nitrate (NO) reabsorption and the effects of furosemide on the renal handling of NOx in anesthetized dogs, using renal clearance and stop-flow methods. Furosemide (2 mg/kg, i.v.) increased the urinary excretion rates of Na+ (U(Na+)V) and NOx (U(NOx)V) with a reduction of tubular reabsorption rates of Na+ and NOx. During inhibition of renal nitric oxide (NO) synthesis by an intrarenal infusion of L-nitro arginine (30 microg/kg-min), furosemide also increased U(NOx)V and decreased tubular reabsorption rate of NOx from 96.5+/-0.8% to 86.6+/-1.7%. An intravenous infusion of 10% mannitol (0.5 ml/kg-min) also increased both U(Na+)V and U(NOx)V. In addition, after furosemide administration or mannitol infusion. U(NOx)V was correlated with U(Na+)V. In stop-flow experiments, the distal dip in NOx curve was observed and the site of the dip in NOx curve was identical to that of Na+ curve. Furosemide shifted upward the U/P(Na+)/U/P(Cr) and U/P(NOx)/U/P(Cr) at the distal dip, indicating inhibition of Na+ and NOx reabsorption at distal tubules. These results indicate that more than 96% of the filtered NOx is reabsorbed in the renal tubules, and that the tubular handling of NOx is very close to that of Na+. In addition, the stop-flow experiments demonstrate that furosemide inhibited the reabsorption of NOx as well as Na+ at the distal tubule.

Anesthesia↗
PubMed1998

Furosemide and digoxin inhibit thiamine uptake in cardiac cells.

Heart cells in culture were used to clarify whether furosemide or digoxin cause thiamine deficiency and if so, by what mechanism. The intracellular level of thiamine pyrophosphate gradually decreased, with a half-life of 16-19 days, after treatment of cardiac cells with furosemide or digoxin. When thiamine was excluded from the growth medium, thiamine pyrophosphate levels gradually decreased, with a half-life of 5-6 days. No additive effect was observed in the presence of the above drugs when thiamine was excluded from the medium. Thiamine uptake by cardiac cells grown in a thiamine-free medium for 7 days decreased significantly in the presence of furosemide or digoxin. The effect of furosemide or digoxin on thiamine uptake was found to be dose dependent. Co-administration of furosemide and digoxin to the cardiac cell cultures resulted in an additive effect on thiamine uptake. Our results demonstrate that furosemide and digoxin inhibit thiamine uptake by cardiac cells in culture and may therefore cause thiamine deficiency in patients undergoing chronic treatment with these drugs.

Animals↗
PubMed1985

Furosemide decreases ventilation in young rabbits.

To test the hypothesis that furosemide would cause metabolic alkalosis and thus alveolar hypoventilation, normal rabbit pups were given either furosemide (4 mg/kg/day) or saline solution for the first 8 to 10 days of life. Pups given furosemide developed primary metabolic alkalosis and reduced ventilation, which resulted in secondary respiratory acidosis. Lung compliance was improved by furosemide, and the ventilatory response to CO2 was unaffected. KCl injection in alkalotic pups increased ventilation and decreased pH. The data show that conventional doses of furosemide can (1) cause metabolic alkalosis and reduce ventilation; (2) increase the PaCO2, which reflects changes in acid-base status and not changes in lung function; and (3) increase lung compliance, perhaps by decreasing lung water. When these effects occur in infants with chronic lung disease, the beneficial effect of furosemide may be obscured.

Acidosis, Respiratory↗
PubMed1986

Short- and long-term effects of furosemide on lung function in infants with bronchopulmonary dysplasia.

Although furosemide improves lung mechanics in some infants with broncho-pulmonary dysplasia (BPD), this may not be important unless gas exchange also improves. To determine the relationship between improvement in mechanics and improvement in gas exchange, the short- and long-term effects of furosemide therapy were studied in 16 spontaneously breathing infants with severe BPD who were both oxygen dependent and hypercarbic (mean PCO2 54 +/- 11 torr). Each infant was examined at least three times: before furosemide therapy, 1 hour after the first dose of furosemide, and after a 6- to 10-day course. Ten of the 16 infants were also examined three times during a 7-day control period. Transcutaneous PO2 and PCO2, esophageal pressure, air flow, and tidal volume were measured. Pulmonary resistance, lung compliance, and the alveolar to skin PO2 difference were calculated. After a single dose of furosemide, only compliance significantly improved. After prolonged therapy, compliance, resistance, and oxygenation significantly improved in the group as a whole, but better oxygenation was achieved in only six of 16 infants. tcPCO2 was unaffected by long-term furosemide therapy, but in all infants with decreased tcPCO2 1 hour after a single dose, there was sustained decrease in PCO2 after prolonged therapy. Changes in gas exchange were not explained by changes in lung mechanics. These data indicate that long-term diuretic therapy can improve the mechanical properties of the lungs of spontaneously breathing infants with BPD, but that gas exchange is usually unaffected.

Airway Resistance↗
PubMed1988

Furosemide pharmacokinetics in very low birth weight infants.

The pharmacokinetics of furosemide were studied longitudinally during long-term administration in 10 very low birth weight infants with bronchopulmonary dysplasia. Mean birth weight of the infants was 829 +/- 217 g, mean gestational age at birth was 26.6 +/- 2.9 weeks, and mean postnatal age at the start of therapy was 2.4 +/- 1.0 weeks. Serial determinations of furosemide pharmacokinetic parameters were performed during 2 weeks to 3 months of long-term therapy. Plasma half-life was prolonged in infants less than 31 weeks postconceptional age (gestational + postnatal age), frequently exceeding 24 hours. All infants less than 29 weeks postconceptional age whose dosing schedule was once every 12 hours accumulated furosemide to potentially ototoxic levels. Furosemide renal clearance increased and plasma half-life decreased in association with increasing postconceptional age. Furosemide secretory clearance was very low in patients less than 31 weeks postconceptional age, resulting in a reliance on glomerular filtration to deliver drug to its main site of action within the lumen of the loop of Henle. Thus elevated plasma levels may be required to ensure adequate luminal delivery and adequate diuresis in these infants with low secretory clearance. Nevertheless, the current dosing schedule (once every 12 hours) of furosemide should be modified to once every 24 hours in infants of low postconceptional age to avoid possible toxic effects.

Age Factors↗
PubMed1995

Improved hypothermic preservation of rat hearts by furosemide.

The effect of furosemide, a blocker of the Na+/K+/Cl- cotransporter, on hypothermic preservation of rat hearts was studied with use of the Langendorff perfusion system and electron microscopy. Furosemide significantly improved the mechanical recovery and the coronary flow of the hearts preserved for 8 hours in St. Thomas' Hospital cardioplegic solution at a temperature of 4 degrees C. Furosemide at the concentration of 100 mumol/L was found to have an optimal effect, whereas at high concentrations (1000 mumol/L) it was found to have toxic effects. In addition, furosemide reduces the time elapsed between the end of the preservation time and the resumption of myocardial contractions. Ultrastructural evaluations were done in which the presence of swollen mitochondria was chosen as a criterion of hypothermic ischemic damage to the myocardium. Morphometric analysis indicated that the mitochondrial volume of hearts stored for 8 hours in St. Thomas' Hospital cardioplegic solution increased by 72% as compared with the mitochondrial volume of hearts that were not exposed to the hypothermic ischemic conditions (control group). The addition of 100 mumol/L furosemide to the cardioplegic solution resulted in a significant reduction of mitochondrial swelling during the period of 8 hours' storage, which amounted only to 28% as compared with the figure for the control group. The reduction of mitochondrial swelling by furosemide and the improved mechanical and coronary flow recoveries are thought to be related to the blocking of the sarcolemmal Na+/K+/Cl- cotransporter and consequently the reduction of the Na+ influx during hypothermic ischemic storage.

Animals↗
PubMed1994

Effect of furosemide and intravenous normal saline fluid load upon the renal resistive index in nonobstructed kidneys in children.

Recent literature has shown that relative to baseline the renal resistive index remains unchanged in nonobstructed kidneys and increases in obstructed kidneys after administration of furosemide. To our knowledge the effect upon the renal resistive index of furosemide administered in conjunction with intravenous normal saline fluid load has not been reported. We evaluated the renal resistive index in 13 nonobstructed kidneys in 8 children 6 to 18 years old before and after furosemide and intravenous normal saline fluid load. The mean resistive index decreased from baseline (mean decrease was 0.06 +/- 0.06 standard deviation), with the observation of a resistive index decrease significant to p < 0.005). It appears likely that the combination of an intravenous normal saline fluid load and furosemide caused the resistive index decrease, since a decrease was not observed with furosemide alone; however, these results cannot exclude the possibility that the resistive index decrease was due to the intravenous normal saline fluid load alone. Nonetheless, these data are important since they may provide the foundation for the development of a pharmacologically challenged Doppler sonographic examination using furosemide and intravenous normal saline fluid load to evaluate better potentially obstructed kidneys.

Adolescent↗
PubMed2000

Effects of hydrochlorothiazide and furosemide diuretics on human bone marrow stromal osteoprogenitor cells.

Thiazide diuretics have been shown to decrease bone loss and improve bone mineral density, while long-term furosemide therapy has been suggested to decrease bone mineral content. However, the direct effects of these diuretics on osteoblastic cells are not well established. Some investigators have reported direct effects of thiazides on osteoblastic cells but the results remain controversial, and there are few data about the direct effect of furosemide on osteoblastic cells. We investigated the effects of hydrochlorothiazide (HCTZ) and furosemide on proliferation, alkaline phosphatase activity, osteocalcin, and interleukin-6/interleukin-11 (IL-6/IL-11) secretion in cultured normal human bone marrow stromal osteoprogenitor cells (hBMSCs). Treatment with HCTZ or furosemide for 24 hours in the concentration range of 10(-6) to 10(-4) mol/L did not affect 3H-thymidine incorporation in hBMSCs. Cellular alkaline phosphatase activity and osteocalcin production were not changed significantly by treatment with HCTZ or furosemide (up to 10(-4) mol/L) during culture. There was also no significant difference in IL-6 and IL-11 production in hBMSCs. These results suggested that HCTZ or furosemide had no significant direct effect on proliferation, alkaline phosphatase activity, osteocalcin, and IL-6/IL-11 production in hBMSCs, and the effects of these diuretics on bone mass may be related to the indirect action on calcium balance.

Alkaline Phosphatase↗
PubMed1996

Effect of acetazolamide on cough induced by low-chloride-ion solutions in normal subjects: comparison with furosemide.

BACKGROUND: The antitussive activity of inhaled furosemide has been attributed to its blocking effect on the Na(+)-2Cl(-)-K+ cotransporter. It is likely that the antitussive activity of inhaled diuretics is more complex because amiloride, a diuretic that has no effect on the Na(+)-2Cl(-)-K+ cotransporter, also shows a significant effect against cough induced by low-chloride-ion solutions. Apart from pharmacokinetics of inhaled diuretics, this activity could also depend on the inhibition of carbonic anhydrase. OBJECTIVES: We therefore studied the effect of inhaled acetazolamide, a selective inhibitor of carbonic anhydrase activity, on cough induced by the inhalation of different chloride ion solutions in a group of normal subjects. This was compared with the antitussive effect of furosemide. In addition, we attempted to determine whether the effect of acetazolamide is dose-dependent. METHODS: Cough challenge consisted of consecutive inhalations of four solutions having decreasing concentrations of chloride ions (150, 75, 37.5 and 0 mmol/L). Nine normal subjects underwent the cough challenge 5 minutes after the inhalation of saline placebo, acetazolamide (500 mg), and furosemide (30 mg) according to a randomized, double-blind study design. A group of six subjects were challenged according to the same procedure and study design, after the inhalation of saline placebo and of two doses of acetazolamide (250 mg and 500 mg). RESULTS: Inhaled acetazolamide significantly reduced cough response to 37.5 and 0 mmol/L chloride solutions compared with placebo (p less than 0.015 and p less than 0.015, respectively). Furosemide showed a similar protective effect (p less than 0.015 and p less than 0.025, respectively). Acetazolamide provided a significantly better protective effect than furosemide (p less than 0.025 and p less than 0.015, respectively). The antitussive activity of the two doses of acetazolamide was not statistically different. CONCLUSION: These results demonstrate that inhaled acetazolamide, a selective inhibitor of carbonic anhydrase, attenuates cough induced by low-chloride-ion solutions in normal subjects. At the applied doses, its antitussive activity is slightly greater than furosemide. This finding suggests that the inhibition of carbonic anhydrase activity is likely involved in modulating changes caused by absence of a chloride ion in the airway microenvironment of human beings.

Acetazolamide↗
PubMed1985

Sulindac and indomethacin suppress the diuretic action of furosemide in patients with cirrhosis and ascites: evidence that sulindac affects renal prostaglandins.

Nonsteroidal anti-inflammatory drugs (NSAID) suppress prostaglandin-dependent renal blood flow and furosemide-induced diuresis in patients with cirrhosis and ascites. Since sulindac may selectively spare inhibition of renal prostaglandins, we evaluated the interactions of acute administration of sulindac or indomethacin with furosemide in 15 patients with cirrhosis and ascites. Prior to furosemide, indomethacin reduced creatinine clearance (by 55%), urinary volume (by 82%), sodium (by 93%), and prostaglandin E2 (by 87%) (all P less than 0.05), whereas sulindac had no effect. However, both drugs reduced furosemide-induced diuresis. Indomethacin appeared slightly more potent in reducing the diuresis (55% v 38%), natriuresis (67% v 52%), and prostaglandin E2 (PGE2) release (81% v 74%). In a similar protocol in healthy subjects, furosemide-induced diuresis and natriuresis were also blunted by both drugs. Thus, under conditions of enhanced prostaglandin activity from furosemide, sulindac does affect renal function. These data suggest that renal function should be monitored in patients with cirrhosis and ascites who receive sulindac as well as other NSAID.

Anti-Inflammatory Agents↗
PubMedDate not supplied

Anaphylaxis to oral furosemide.

Furosemide, one of the most used diuretic drugs, rarely induces type-1 allergic reactions It is included in the non-aromatic sulfonamides but a cross-reactivity mechanism between this group and the sulfonamides antibiotics, has not been clearly demonstrated. A 24-year-old woman, 10 minutes after the intake of one pill of Seguril 40mg experienced oral itching, generalized urticaria, facial angioedema, dyspnea and hypotension. She recovered after the administration of parental adrenaline, methyl-prednisolone and dyphenhydramine. An skin prick test with furosemide (10 mg/ml) was negative. The intradermal skin tests were positive to furosemide (1 %) as well as sulfamethoxazole (0.03 mg/ml), with 10 atopic and non-atopic negative controls. The patient rejected the performance of an oral challenge test with sulfamethoxazole. IgE-mediated reactions to furosemide are infrequent, but it could be the cause of life-threatening reactions. We have reported a case of anaphylaxis after the oral administration of furosemide with a demonstrated hypersensitivity mechanism through the positive intradermal skin test. The previous administration of the drug could probably the mechanism of sensitization, but the positive intradermal test to sulfamethoxazole would open the hypothesis of a cross-reactivity between non-aromatic and antimicrobial sulfonamides. It could be necessary an oral challenge test with furosemide in allergic patients to sulfamides.

Administration, Oral↗
PubMed2002

Rapid analysis of furosemide in human urine by capillary electrophoresis with laser-induced fluorescence and electrospray ionization-ion trap mass spectrometric detection.

Furosemide, a drug that promotes urine excretion, is used in the pharmacotherapy of various diseases and is considered as a doping agent in sports. Using alkaline electrolytes, analysis of furosemide by dodecyl sulfate based micellar electrokinetic capillary chromatography (MECC) and capillary zone electrophoresis (CZE) with laser-induced fluorescence detection (LIF, analyte excitation with the 325 nm line of a HeCd laser) is described. Data produced by injection of plain or diluted patient urines are confirmed with those obtained via analysis of urinary solid-phase extracts. CZE-LIF and MECC-LIF are thereby shown to permit unambiguous recognition of furosemide in urines collected after ingestion of therapeutic doses of this drug. This is in contrast to solute detection via UV absorbance for which the extraction of furosemide is required. MECC based electropherograms are somewhat more complex compared to those obtained by CZE-LIF, this suggesting that the latter approach is more suitable for rapid screening of urines with direct sample injection and LIF detection. Alternatively, capillary electrophoresis with negative electrospray ionization-ion-trap tandem mass spectrometry (CE-MS2) is shown to permit the direct confirmation of furosemide in human urine. This approach is based upon the monitoring of the m/z 329.3-->4m/z 285.2 precursor-product ion transition. CZE-LIF and CE-MS2 with injection of plain or diluted urine represent simple, rapid and attractive urinary screening and confirmation assays for furosemide in patient urines.

Diuretics↗