Skip to Content


Class: Loop Diuretics
VA Class: CV702
Chemical Name: 3-(Aminosulfonyl)-5-(butylamino)-4-phenoxybenzoic acid
Molecular Formula: C17H20N2O5S
CAS Number: 28395-03-1

Medically reviewed by Last updated on Apr 15, 2019.


  • Bumetanide is a potent diuretic which, if given in excessive amounts, can lead to a profound diuresis with water and electrolyte depletion.4

  • Careful medical supervision is required; adjust dosage selection and titration according to the individual patient’s needs.4 (See Dosage and Administration.)


A sulfonamide loop-type diuretic and antihypertensive agent.4 1200

Uses for Bumetanide


Management of edema associated with heart failure or hepatic or renal disease (including nephrotic syndrome).3 4 524

May be effective in some patients whose condition is unresponsive or refractory to other diuretics.5 47 49 52

Considered a diuretic of choice for most patients with heart failure.524

Most experts state that all patients with symptomatic heart failure who have evidence for, or a history of, fluid retention generally should receive diuretic therapy in conjunction with moderate sodium restriction, an agent to inhibit the renin-angiotensin-aldosterone (RAA) system (e.g., ACE inhibitor, angiotensin II receptor antagonist, angiotensin receptor-neprilysin inhibitor [ARNI]), a β-adrenergic blocking agent (β-blocker), and in selected patients, an aldosterone antagonist.524 700 713

Short- and long-term management of edema and ascites associated with hepatic disease (e.g., cirrhosis).2 31 36 48 49 50

Management of postoperative or premenstrual edema and edema associated with disseminated carcinoma.5


Management of hypertension, alone or in combination with other classes of antihypertensive agents.5 92 94 113 127 128 1200

Not considered a preferred agent for initial management of hypertension according to current evidence-based hypertension guidelines;501 502 503 504 other agents (i.e., ACE inhibitors, angiotensin II receptor antagonists, calcium-channel blockers, thiazide diuretics) are preferred for initial management.501 502 503 504 1200

Some experts state that loop diuretics (e.g., bumetanide, furosemide, torsemide) are preferred over thiazides in patients with moderate to severe chronic kidney disease (CKD)502 504 1200 or symptomatic heart failure.524 1200

Individualize choice of therapy; consider patient characteristics (e.g., age, ethnicity/race, comorbidities, cardiovascular risk) as well as drug-related factors (e.g., ease of administration, availability, adverse effects, cost).501 502 503 504 515 1200 1201

A 2017 ACC/AHA multidisciplinary hypertension guideline classifies BP in adults into 4 categories: normal, elevated, stage 1 hypertension, and stage 2 hypertension.1200 (See Table 1.)

Source: Whelton PK, Carey RM, Aronow WS et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018;71:e13-115.

Individuals with SBP and DBP in 2 different categories (e.g., elevated SBP and normal DBP) should be designated as being in the higher BP category (i.e., elevated BP).

Table 1. ACC/AHA BP Classification in Adults1200


SBP (mm Hg)

DBP (mm Hg)









Hypertension, Stage 1




Hypertension, Stage 2




The goal of hypertension management and prevention is to achieve and maintain optimal control of BP.1200 However, the BP thresholds used to define hypertension, the optimum BP threshold at which to initiate antihypertensive drug therapy, and the ideal target BP values remain controversial.501 503 504 505 506 507 508 515 523 526 530 1200 1201 1207 1209 1222 1223 1229

The 2017 ACC/AHA hypertension guideline generally recommends a target BP goal (i.e., BP to achieve with drug therapy and/or nonpharmacologic intervention) of <130/80 mm Hg in all adults regardless of comorbidities or level of atherosclerotic cardiovascular disease (ASCVD) risk.1200 In addition, an SBP goal of <130 mm Hg generally is recommended for noninstitutionalized ambulatory patients ≥65 years of age with an average SBP of ≥130 mm Hg.1200 These BP goals are based upon clinical studies demonstrating continuing reduction of cardiovascular risk at progressively lower levels of SBP.1200 1202 1210

Other hypertension guidelines generally have based target BP goals on age and comorbidities.501 504 536 Guidelines such as those issued by the JNC 8 expert panel generally have targeted a BP goal of <140/90 mm Hg regardless of cardiovascular risk, and have used higher BP thresholds and target BPs in elderly patients501 504 536 compared with those recommended by the 2017 ACC/AHA hypertension guideline.1200

Some clinicians continue to support previous target BPs recommended by JNC 8 due to concerns about the lack of generalizability of data from some clinical trials (e.g., SPRINT study) used to support the 2017 ACC/AHA hypertension guideline and potential harms (e.g., adverse drug effects, costs of therapy) versus benefits of BP lowering in patients at lower risk of cardiovascular disease.1222 1223 1224 1229

Consider potential benefits of hypertension management and drug cost, adverse effects, and risks associated with the use of multiple antihypertensive drugs when deciding a patient's BP treatment goal.1200 1220 1229

For decisions regarding when to initiate drug therapy (BP threshold), the 2017 ACC/AHA hypertension guideline incorporates underlying cardiovascular risk factors.1200 1207 ASCVD risk assessment is recommended by ACC/AHA for all adults with hypertension.1200

ACC/AHA currently recommend initiation of antihypertensive drug therapy in addition to lifestyle/behavioral modifications at an SBP ≥140 mm Hg or DBP ≥90 mm Hg in adults who have no history of cardiovascular disease (i.e., primary prevention) and a low ASCVD risk (10-year risk <10%).1200

For secondary prevention in adults with known cardiovascular disease or for primary prevention in those at higher risk for ASCVD (10-year risk ≥10%), ACC/AHA recommend initiation of antihypertensive drug therapy at an average SBP ≥130 mm Hg or an average DBP ≥80 mm Hg.1200

Adults with hypertension and diabetes mellitus, CKD, or age ≥65 years are assumed to be at high risk for cardiovascular disease; ACC/AHA state that such patients should have antihypertensive drug therapy initiated at a BP ≥130/80 mm Hg.1200 Individualize drug therapy in patients with hypertension and underlying cardiovascular or other risk factors.502 1200

In stage 1 hypertension, experts state that it is reasonable to initiate drug therapy using the stepped-care approach in which one drug is initiated and titrated and other drugs are added sequentially to achieve the target BP.1200 Initiation of antihypertensive therapy with 2 first-line agents from different pharmacologic classes recommended in adults with stage 2 hypertension and average BP >20/10 mm Hg above BP goal.1200

Bumetanide Dosage and Administration


  • Excessive fluid and electrolyte loss may be minimized by monitoring the patient carefully and by initiating therapy with small doses, adjusting dosage carefully, and using an intermittent dosage schedule if possible.4 (See Boxed Warning.)

  • For the management of fluid retention associated with heart failure, experts state that diuretics should be administered at a dosage sufficient to achieve optimal volume status and relieve congestion without inducing excessively rapid reduction in intravascular volume, which could result in hypotension, renal dysfunction, or both.524

  • Supplemental therapy with potassium chloride or potassium-sparing diuretics (e.g., spironolactone) may be necessary for the prevention of hypokalemia and/or metabolic alkalosis in some patients.4

Monitoring and BP Treatment Goals

  • Monitor BP regularly (i.e., monthly) during therapy and adjust dosage of the antihypertensive drug until BP controlled.1200

  • If unacceptable adverse effects occur, discontinue drug and initiate another antihypertensive agent from a different pharmacologic class.1216

  • Assess patient's renal function and electrolytes 2–4 weeks after initiation of diuretic therapy.1200

  • If adequate BP response not achieved with a single antihypertensive agent, either increase dosage of single drug or add a second drug with demonstrated benefit and preferably a complementary mechanism of action (e.g., ACE inhibitor, angiotensin II receptor antagonist, calcium-channel blocker).1200 1216 Many patients will require ≥2 drugs from different pharmacologic classes to achieve BP goal; if goal BP still not achieved with 2 antihypertensive agents, add a third drug.1200 1216 1220


Administer orally, IV, or IM.4

Oral Administration

Administer orally as a single daily dose in the morning.4 May be preferable to administer single daily dose in the evening for a greater diuretic effect.24 67 81 May administer on alternate days or on 3 or 4 consecutive days alternating with drug-free periods of 1 or 2 days.4

For optimum therapeutic effect in some patients, may administer twice daily (morning and evening).67

Food may delay absorption.22

IV or IM Administration

For solution and drug compatibility information, see Compatibility under Stability.

IV or IM administration may be used in patients unable to take oral medication or who have impaired GI absorption; resume oral administration as soon as possible.4

Rate of Administration

For direct IV injection, administer slowly over a period of 1–2 minutes.4


For IV infusion, dilute in 5% dextrose, 0.9% sodium chloride, or lactated Ringer’s injection; use solutions within 24 hours.4


Individualize dosage according to individual requirements and response.4

Since the diuretic response following oral or parenteral administration is similar, dosage for oral, IV, or IM administration is identical.4

Manufacturer states that bumetanide may be substituted for furosemide in furosemide-allergic patients at approximately a 1:40 ratio (cross-sensitivity between the drugs does not appear to occur).4 49 (See Sensitivity Reactions under Cautions.)

Pediatric Patients

Heart Failure

Safety and efficacy not established.4

0.015 mg/kg on alternate days to 0.1 mg/kg daily has been used in a limited number of children with heart failure.42

In infants 4 days to 6 months of age, maximal diuretic effect was observed at a dosage of 0.035–0.04 mg/kg.a



Initially, 0.5–2 mg daily.4 Repeat dose at 4- to 5-hour intervals until desired response is obtained or maximum dosage of 10 mg daily is reached.4

For maintenance therapy, effective dose may be administered intermittently.4 (See Administration under Dosage and Administration.)

For management of fluid retention associated with heart failure, some experts recommend initiating at a low dosage (e.g., 0.5–1 mg once or twice daily) and increasing dosage (maximum 10 mg daily) until urine output increases and weight decreases, generally by 0.5–1 kg daily.524

IV or IM

Initially, 0.5–1 mg.4 Repeat dose at 2- to 3-hour intervals until desired diuretic response is obtained or a maximum dosage of 10 mg daily is reached.4


Initially, 0.5 mg daily.92 94 111

Some experts state that usual dosage range is 0.5–2 mg daily administered in 2 divided doses.1200

Prescribing Limits



Maximum recommended by manufacturer and some experts: 10 mg daily.4 524

IV or IM

Maximum recommended by manufacturer: 10 mg daily.4

Special Populations

Hepatic Impairment


Use minimum effective dosage; titrate carefully.4

Renal Impairment

Oral or IV

Up to 20 mg daily has been administered.37 55 IV doses >2 mg needed to achieve a diuretic response in patients with Clcr <5 mL/minute.2 54 High dosages may be needed to produce an adequate diuretic response in patients with severe renal impairment (i.e., GFR <10 mL/minute).5

Geriatric Patients

Select dosage with caution because of age-related decreases in hepatic, renal, and/or cardiac function and concomitant disease and drug therapy.a

Cautions for Bumetanide


  • Anuria.4

  • Marked increases in BUN or Scr or development of oliguria during treatment of progressive renal disease.4

  • Hepatic coma or severe electrolyte depletion, until condition is improved or corrected.4

  • Known hypersensitivity to bumetanide or any ingredient in the formulation.4



Fluid, Electrolyte, and Cardiovascular Effects

Careful etiologic diagnosis should precede use of any diuretic.d Titrate dosage carefully; excessive dosage, administration frequency, or prolonged therapy may lead to profound water loss, electrolyte depletion, dehydration, reduction in blood volume, and circulatory collapse with the possibility of vascular thrombosis and embolism, especially in geriatric patients.4 (See Boxed Warning.)

Observe carefully for signs of electrolyte depletion, especially hypokalemia.4 Excessive fluid and electrolyte loss may be minimized by careful monitoring and initiating therapy with small doses, careful dosage adjustment, and an intermittent dosage schedule if possible.4

Hypokalemia may occur; evaluate serum potassium concentration periodically.4 Hypokalemia is particularly likely and important to prevent in patients with hyperaldosteronism and normal renal function, hepatic cirrhosis and ascites, potassium-losing renal diseases, or certain diarrheal conditions and may require particular attention in patients with heart failure receiving cardiac glycosides and diuretics, those with a history of ventricular arrhythmias, and those with other conditions in which hypokalemia represents a risk.4 (See Hepatic Impairment under Cautions.)

Periodic determination of other serum electrolyte concentrations recommended for patients receiving high dosages or chronic therapy, especially when sodium intake is restricted.4 If excessive diuresis and/or electrolyte abnormalities occur, discontinue therapy or reduce dosage until corrected.76 81 82


Produces ototoxicity in animals at high dosages.4 Serum concentrations associated with ototoxicity in humans unlikely; consider possibility of ototoxicity following IV administration, especially at high dosages,4 after too rapid administration,81 in patients with impaired renal function, and/or in patients receiving other ototoxic drugs (e.g., aminoglycosides).4 (See Specific Drugs under Interactions.)


Rare postmarketing experience reports; monitor regularly.4

Sensitivity Reactions


Patients allergic to sulfonamides may be hypersensitive to bumetanide; use with extreme caution.4 Does not appear to exhibit cross-sensitivity in patients allergic to furosemide.4 69 2

General Precautions

Electrolyte Effects

Hypomagnesemia, hypocalcemia, and/or hypophosphatemia may occur.4 31

Endocrine Effects

Possible effects on glucose metabolism should be considered.4 Changes in plasma insulin, glucagon, or growth hormone concentration or in glucose tolerance or diabetic control generally have not been observed; diuretic-induced hyperglycemia occurs rarely.2 3 4 5 18 19 24 83 84 May result from potassium depletion, which has been associated with impaired insulin secretion.2 3 4 5 18 19 83 84

Other Effects

Blood dyscrasias (especially thrombocytopenia), liver damage, or idiosyncratic reactions have been reported occasionally.4

Hyperuricemia may occur; most reported cases have been asymptomatic.4 25 31 32 43

Specific Populations


Category C.4


Not known whether bumetanide is distributed into milk.4 Use not recommended.4

Pediatric Use

Safety and efficacy not established in children <18 years of age.4

Has been used effectively as a diuretic for up to 40 weeks in a limited number of infants 2 weeks to 7 months of age with congenital heart disease and heart failure.42

Use with caution in critically ill or jaundiced neonates at risk for kernicterus; in vitro studies indicate bumetanide may displace bilirubin from albumin.4 (See Distribution: Special Populations, under Pharmacokinetics.)

Elimination appears to be slower in neonates than in adults, possibly because of immature renal and hepatobiliary functions.4 (See Elimination: Special Populations, under Pharmacokinetics.)

Geriatric Use

Response in patients ≥65 years of age does not appear to differ from that in younger adults; however, use with caution due to greater frequency of decreased hepatic, renal, and/or cardiac function and of concomitant disease and drug therapy observed in geriatric patients.4 (See Fluid, Electrolyte, and Cardiovascular Effects under Cautions.) Monitor renal function.4

Hepatic Impairment

Use with caution in patients with hepatic cirrhosis and ascites; sudden alterations in electrolyte balance may precipitate hepatic encephalopathy and coma.4 Therapy in such patients is best initiated in the hospital with small doses and careful monitoring of clinical status and electrolyte balance.4 Supplemental potassium and/or concomitant potassium-sparing diuretics (e.g., spironolactone) may be used to prevent hypokalemia and metabolic alkalosis.4 31 48 50

Renal Impairment

Patients with renal impairment may require high dosages to achieve an adequate diuretic response.5 (See Renal Impairment under Dosage and Administration.)

The risk of adverse effects (e.g., ototoxicity) at high dosages should be considered.4 (See Ototoxicity under Cautions.)

Common Adverse Effects

Muscle cramps, dizziness, hypotension, headache, nausea, encephalopathy, hyperuricemia, hypochloremia, hypokalemia, azotemia, hyponatremia, increased serum creatinine, hyperglycemia.4 38 81 82

Interactions for Bumetanide

Specific Drugs




Anticoagulants, oral (e.g., warfarin)

Plasma prothrombin activity or warfarin metabolism not affected 4 65 66

Antihypertensive agents

Additive antihypertensive effect3 4

Reduction in dosage of both drugs may be required.3 4

Concomitant therapy generally used to therapeutic advantage; orthostatic hypotension may occur.34

Cardiac glycosides (e.g., digoxin)

Possible electrolyte disturbances (e.g., hypokalemia, hypomagnesemia) may predispose to digitalis toxicity, possibly fatal cardiac arrhythmias3 4 77 79

Renal excretion and serum digoxin concentrations not affected3 4 59

Monitor electrolytes; correct hypokalemia4 79 80


Increased diuretic and natriuretic effects3 25

Diuretics, potassium- sparing (e.g., amiloride, spironolactone, triamterene)

Possible reduction in potassium loss3 25

Concomitant therapy may be used to therapeutic advantage3 25


Decreased diuretic and natriuretic effect3 4 60 61 62 78

Concomitant therapy not recommended4

If concomitant therapy is necessary, increased bumetanide dosage may overcome decreased diuretic effect82 .

Other drugs causing potassium loss (corticosteroids, corticotropin, amphotericin B)79 81

Additive hypokalemic effects 81

Monitor electrolytes; correct hypokalemia4 81


Reduced renal clearance of lithium and increased risk of lithium toxicity3 4

Concomitant use generally contraindicated; if concomitant therapy is necessary, monitor serum lithium concentrations and adjust dosage3 4 81

Nondepolarizing neuromuscular blocking agents (e.g., atracurium besylate, tubocurarine chloride)

Potential for prolonged neuromuscular blockade, possibly due to potassium depletion and/or decreased urinary excretion of neuromuscular blocking agent79 85 86

Clinical importance unknown; use with caution81

Nephrotoxic drugs

Possible increased nephrotoxic effects; no clinical experience to date 4

Avoid concomitant use4

Ototoxic drugs (e.g., aminoglycoside antibiotics, cisplatin)

Possible additive ototoxic effect, especially in patients with impaired renal function3 4

Avoid concomitant parenteral administration of bumetanide and aminoglycoside antibiotics, except in life-threatening conditions4


Decreased diuretic and natriuretic effects, inhibition of bumetanide-induced increase in plasma renin activity3 4 8 62 63

Avoid concomitant use4

Bumetanide Pharmacokinetics



Rapidly and almost completely (85–95%)2 3 20 21 22 absorbed following oral administration;22 23 peak plasma concentrations generally attained within 0.5–2 hours.3 13 14 20 21 22 23

Appears to be completely absorbed following IM administration.2


Diuresis begins within 30–60 minutes following oral administration,3 4 about 40 minutes following IM administration,73 and within a few minutes following IV administration.4 Peak diuretic activity generally occurs within 1–2 hours following oral or IM administration14 20 22 24 25 73 and within 15–30 minutes after IV administration.4 21 22


Diuresis is dose-dependent and generally complete within 4–6 hours following oral or IM administration.3 4 14 20 24 25 73

Following IV administration, diuresis generally persists for 2–3 hours.21


Limited data suggest food may delay GI absorption.22

Special Populations

Bioavailability appears similar in patients with impaired renal or hepatic function.23



Distribution has not been fully characterized.2 3 20

Not known whether bumetanide crosses the blood-brain barrier or the placenta or is distributed into milk.3 4

Bumetanide and its metabolites are distributed into bile.3 4 20 Following oral administration of radiolabeled bumetanide in one patient with a biliary T tube in place, 1.8% of the dose was distributed into bile as unchanged drug and 12.6% as metabolites.20

Does not appear to bind to erythrocytes.2 3 21

Following IV administration in healthy adults, the steady-state volume of distribution (Vss) ranged from 9.45–19.7 L and the volume of distribution of the central compartment (Vc) ranged from 3.26–5.84 L.14 21 22 29

Plasma Protein Binding

Approximately 93–96%.21 29

Special Populations

Following IV administration in neonates, the mean volume of distribution ranged from 0.26–0.38 L/kg.4

May increase serum concentrations of free (unbound) bilirubin by displacement from albumin when administered to critically ill neonates.4 28

Protein binding may be decreased in patients with renal impairment; binding appears to be correlated with plasma albumin concentration.91

Vss may be increased in patients with renal impairment.91

Vss may be decreased in patients with hepatic impairment.23



Bumetanide is partially metabolized by oxidation in the liver to at least 5 metabolites.3 20 21 Major urinary metabolite is the 3′-alcohol derivative.20 The major metabolite excreted in bile and/or feces is the 2′-alcohol derivative.20 Minor metabolites include the 4′-alcohol, N-desbutyl, and 3′-acid derivatives.20

Metabolites in urine and bile are present as conjugates, principally glucuronide conjugates.20 Conjugates of bumetanide and its metabolites do not appear in feces.20

Elimination Route

Bumetanide and its metabolites are excreted principally in urine.3 4 20 21 22 29 Renal excretion appears to occur mainly via glomerular filtration;3 22 29 91 tubular secretion also may occur.22 29 91

Following oral or IV administration in healthy adults, about 80% of a dose is excreted in urine and 10–20% in feces within 48 hours;3 20 21 29 about 50% of a dose is excreted unchanged in urine.3 20 21 29 Excreted in feces almost completely as metabolites, apparently via biliary elimination;20 less than 2% of a dose is excreted unchanged in feces within 48 hours.20


1–1.5 hours in healthy adults following oral administration.3 4 20

Plasma concentrations generally decline in a monophasic or biphasic manner;2 14 20 21 22 however, plasma concentrations may decline in a triphasic manner following IV administration.22 29

Following IV administration in adults with normal renal and hepatic function, t½α averages 5–6.9 minutes, t½β averages 46–47 minutes, and t½γ averages 3.1–3.4 hours.22 29

Special Populations

Clearance decreased in patients with impaired renal function, with or without concurrent hepatic impairment;29 91 101 in patients with only renal impairment, nonrenal clearance of the drug is about 90% or more of total body clearance.29 91 101 Serum concentrations may be higher and the terminal elimination half-life prolonged in patients with impaired renal and/or hepatic function.23 91

In neonates and infants, elimination appears slower than in older pediatric patients and adults, possibly because of immature renal and hepatobiliary functions.4 Mean serum elimination half-life decreased considerably during the first month of life from 6 hours in neonates to 2.4 hours in infants 1 month of age.a Mean serum elimination half-life is 2.5 and 1.5 hours in infants younger than 2 months of age and in those 2–6 months of age, respectively.4 Limited data indicate that the apparent elimination half-life may be prolonged to about 6 hours (with a range up to 15 hours) after IV administration in premature or full-term neonates with respiratory disorders.4





15–30°C in tight, light resistant containers.3 4 95



15–30°C; protect from light.b

If diluted with infusion solution, use within 24 hours of preparation.b


For information on systemic interactions resulting from concomitant use, see Interactions.


Physically and chemically compatible in glass and PVC containers.3 b

Solution CompatibilityHID


Dextrose 5% in water

Sodium chloride 0.9%

Ringer’s injection, lactated

Drug Compatibility
Admixture CompatibilityHID




Dobutamine HCl

Y-Site CompatibilityHID


Allopurinol sodium




Caspofungin acetate

Ceftaroline fosamil

Cisatracurium besylate


Dexmedetomidine HCl

Diltiazem HCl



Etoposide phosphate


Gemcitabine HCl

Granisetron HCl

Hetastarch in lactated electrolyte injection (Hextend)


Melphalan HCl

Meperidine HCl

Micafungin sodium

Milrinone lactate

Morphine sulfate


Pemetrexed disodium

Piperacillin sodium–tazobactam sodium


Remifentanil HCl



Vinorelbine tartrate


Fenoldopam mesylate

Midazolam HCl



  • Loop diuretic with a rapid onset and short duration of action.4

  • Approximately 40 times the diuretic activity of furosemide on a weight basis;2 3 4 5 11 25 relative potency may vary with different dosages and/or routes of administration.3 12 73

  • Decreases electrolyte reabsorption by inhibiting the active chloride and sodium transport systems in the ascending limb of the loop of Henle to inhibit sodium and chloride reabsorption.4 6 7 8 13 51 89

  • Increases urinary excretion of sodium, chloride, potassium, hydrogen, calcium, magnesium, ammonium and possibly phosphate and bicarbonate.3 4 6 7 8 9 10 13 14 15

  • The chloruretic effect of the drug is greater than its natriuretic effect, and its effect on urinary calcium and magnesium excretion is less than that on sodium excretion.3 4 6 7 13 15

  • Increases potassium secretion in the distal renal tubule in a dose-related manner secondary to increased sodium load in the tubule.3 4 5 7 10 72

  • Induces phosphaturia and bicarbonate excretion; appears to inhibit sodium phosphate-linked transport in the proximal renal tubule.2 4 5 6 7 8 9

  • Decreases uric acid excretion and increases serum uric acid concentration.4 7 8 14 25

  • Produces renal vascular dilation and substantially increases renal blood flow.3 7 16

  • Produces variable but substantial increases in plasma renin activity (PRA).13

  • Produces hypotensive effects and decreases body weight resulting from decreased plasma volume.3 4

  • Reduces mean pulmonary venous pressure, left ventricular end-diastolic pressure, mean pulmonary artery pressure, and mean right atrial pressure in patients with valvular heart disease.3

  • Reduces cardiac output, cardiac index, stroke volume, stroke index, and diastolic pressures in patients with coronary artery disease.3

Advice to Patients

  • Importance of informing patients to report any signs and symptoms of electrolyte imbalance (weakness, dizziness, fatigue, faintness, mental confusion, lassitude, muscle cramps, headache, paresthesia, thirst, anorexia, nausea, and/or vomiting) to their clinician.3 75 76 81 82

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.4

  • Importance of women informing their clinician if they are or plan to become pregnant or plan to breast-feed.4

  • Importance of informing patients of other important precautionary information.4 (See Cautions.)


Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name



Dosage Forms


Brand Names




0.5 mg*

Bumetanide Tablets

1 mg*

Bumetanide Tablets

2 mg*

Bumetanide Tablets



0.25 mg/mL*

Bumetanide Injection

AHFS DI Essentials™. © Copyright 2020, Selected Revisions April 15, 2019. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Use is not currently included in the labeling approved by the US Food and Drug Administration.


1. Feit PW. Bumetanide—the way to its chemical structure. J Clin Pharmacol. 1981; 21:531-6.

2. Halstenson CE, Matzke GR. Bumetanide: a new loop diureti. Drug Intell Clin Pharm. 1983; 17:786-97.

3. Roche Laboratories. Bumex comprehensive product information. Nutley, NJ; 1983 Mar.

4. Roche Laboratories. Bumex (bumetanide) tablets and injection prescribing information. Nutley, NJ; 1999 Feb.

5. Flamenbaum W, Friedman R. Pharmacology, therapeutic efficacy, and adverse effects of bumetanide, a new “loop” diuretic. Pharmacotherapy. 1982; 2:213-22.

6. Puschett JB. Renal effects of bumetanide. J Clin Pharmacol. 1981; 21:575-80.

7. Olsen UB. The pharmacology of bumetanide. Acta Pharmacol Toxicol (Copenh). 1977; 41(Suppl. 3):1-24.

8. Lant AF. Effects of bumetanide on cation and anion transport. Postgrad Med J. 1975; 51(Suppl. 6):35-42.

9. Jayakumar S, Puschett JB. Study of the sites and mechanisms of action of bumetanide in man. J Pharmacol Exp Ther. 1977; 201:251-8.

10. Bourke E. Some aspects of the renal action and clinical pharmacology of oral bumetanide in man. Postgrad Med J. 1975; 51(Suppl. 6):23-6.

11. Cohen M. Pharmacology of bumetanide. J Clin Pharmacol. 1981; 21:537-42.

12. Ramsay LE, McInnes GT, Hettiarachchi J et al. Bumetanide and furosemide: a comparison of dose-response curves in healthy men. Br J Clin Pharmacol. 1978; 5:243-7.

13. Velasquez MT, Wan SH, Maronde RF. Bumetanide-induced rise in plasma renin activity. Clin Pharmacol Ther. 1978; 24:186-91.

14. Davies DL, Lant AF, Millard NR et al. Renal action, therapeutic use, and pharmacokinetics of the diuretic bumetanide. Clin Pharmacol Ther. 1974; 15:141-55.

15. Hutcheon DE, Vincent ME, Sandhu RS. Renal electrolyte excretion pattern in response to bumetanide in healthy volunteers. J Clin Pharmacol. 1981; 21:604-9.

16. Higashio T, Abe Y, Tamamoto K. Renal effects of bumetanide. J Pharmacol Exp Ther. 1978; 207:212-20.

17. Sigurd B, Hesse B, Bollerup AC. Investigations with intravenous bumetanide. Postgrad Med J. 1975; 51(Suppl. 6):27-35.

18. Giugliano D, Varricchio M, Cerciello T et al. Bumetanide and glucose tolerance in man. Farmaco Ed Prat. 1980; 35:403-8.

19. Robinson DS, Nilsson CM, Leonard RF et al. Effects of loop diuretics on carbohydrate metabolism and electrolyte excretion. J Clin Pharmacol. 1981; 21:637-46.

20. Halladay SC, Sipes IG, Carter DE. Diuretic effect and metabolism of bumetanide in man. Clin Pharmacol Ther. 1977; 22:179-87.

21. Pentikainen PJ, Penttila A, Neuvonen PJ et al. Fate of [14C]-bumetanide in man. Br J Clin Pharmacol. 1977; 4:39-44.

22. Marcantonio LA, Auld WHR, Skellern GG et al. The pharmacokinetics and pharmacodynamics of bumetanide in normal subjects. J Pharmacokinet Biopharm. 1982; 10:393-409.

23. Marcantonio LA, Auld WHR, Murdock WR et al. The pharmacokinetics and pharmacodynamics of the diuretic bumetanide in hepatic and renal disease. Br J Clin Pharmacol. 1983; 15:245-52.

24. Murdoch WR, Auld WHR. Bumetanide—acute and long-term studies of a new high potency diuretic. Postgrad Med J. 1975; 51(Suppl. 6):64-9.

25. Olesen KH, Sigurd B, Hesse B et al. Diuretic action of bumetanide in congestive heart failure. Postgrad Med J. 1975; 51(Suppl. 6):54-63.

26. Cohen MR, Hinsch E, Vergona R et al. A comparative diuretic and tissue distribution study of bumetanide and furosemide in the dog. J Pharmacol Exp Ther. 1976; 197:697-702.

27. Beermann B, Groschinsky-Grind M. Clinical pharmacokinetics of diuretics. Clin Pharmacokinet. 1980; 5:221-45.

28. Turmen T, Thom P, Louridas T et al. Protein binding and bilirubin displacing properties of bumetanide and furosemide. J Clin Pharmacol. 1982; 22:551-6.

29. Pentikainen PJ, Neuvonen PJ, Kekki M et al. Pharmacokinetics of intravenously administered bumetanide in man. J Pharmacokinet Biopharm. 1980; 8:219-28.

30. Brater DC, Chennavasin P, Day B et al. Bumetanide and furosemide. Clin Pharmacol Ther. 1983; 34:207-13.

31. Herlong HF, Hunter FM, Koff RS et al. A comparison of bumetanide and furosemide in the treatment of ascites: cooperative study. J Clin Pharmacol. 1981; 21:701-5.

32. Nicholson G. Treatment of fluid retention in cirrhosis: a comparison of bumetanide and furosemide. Curr Med Res Opin. 1977; 4:675-9.

33. Cuthbert MF. Reports of adverse reactions with bumetanide. Postgrad Med J. 1975; 51(Suppl. 6):51-2.

34. Stone WJ, Bennett WM, Cutler RE. Long-term bumetanide treatment of patients with edema due to renal disease: cooperative studies. J Clin Pharmacol. 1981; 21:587-90.

35. Kourouklis C, Christensen O, Augoustakis D. Bumetanide in congestive heart failure. Curr Med Res Opin. 1976; 4:422-31.

36. Ring-Larsen H. Bumetanide in the treatment of hepatic ascites: a short and long-term study. Acta Med Scand. 1974; 195:411-4.

37. Barclay JE, Lee HA. Clinical and pharmacokinetic studies on bumetanide in chronic renal failure. Postgrad Med J. 1974; 51(Suppl. 6):43-6.

38. Tuzel IH. Comparison of adverse reactions to bumetanide and furosemide. J Clin Pharmacol. 1981; 21:615-9.

39. Handler B, Dhingra RC, Rosen KMR. Bumetanide: a new diuretic. Results of clinical efficacy and safety in patients with congestive heart failure. J Clin Pharmacol. 1981; 21:691-6.

40. Brown RD, Manno JE, Daigneault EA et al. Comparative actue ototoxicity of intravenous bumetanide and furosemide in the pure-bred beagle. Toxicol Appl Pharmacol. 1979; 48:157-69.

41. Bourke E. Some aspects of the renal action and clinical pharmacology of oral bumetanide in man. Postgrad Med J. 1975; 51(Suppl. 6):23-6.

42. Ward OC, Lam LK. Bumetanide in heart failure in infancy. Arch Dis Child. 1977; 52:877-82.

43. Murchison LE, Bewsher PD, Seymour R. Lack of effect of bumetanide on body potassium content in hypertension. Br J Clin Pharmacol. 1975; 2:87-91.

44. Hutcheon D, Vincent ME, Sandhu RS. Clinical use of diuretics in congestive heart failure. J Clin Pharmacol. 1981; 21:668-72.

45. Dixon DW, Barwolf-Gohlke C, Gunnar RM. Comparative efficacy and safety of bumetanide and furosemide in long-term treatment of edema due to congestive heart failure. J Clin Pharmacol. 1981; 21:680-7.

46. Konecke LL. Clinical trial of bumetanide versus furosemide in patients with congestive heart failure. J Clin Pharmacol. 1981; 21:688-90.

47. Pines A, Sreedharan KS, Nandi AR et al. A clinical assessment of bumetanide in patients not responding to other diuretics. Br J Clin Pract. 1974; 28:311-3.

48. Moult PJA, Lunzer MR, Trash DB et al. Use of bumetanide in the treatment of ascites due to liver disease. Gut. 1974; 15:988-92.

49. Koff RS. The effects of a single, intravenous dose of bumetanide versus furosemide in patients with ascites and edema due to alcoholic liver disease. J Clin Pharmacol. 1981; 21:706-11.

50. Iber FL, Baum RA. Bumetanide in refractory ascites of cirrhosis of the liver: a comparison with furosemide. J Clin Pharmacol. 1981; 21:697-700.

51. Imai M. Effect of bumetanide and furosemide on the thick ascending limb of Henle’s loop of rabbits and rats perfused in vitro. Eur J Pharmacol. 1977; 41:409-16.

52. Asbury MJ, Gatenby PBB, O’sullivan S et al. Bumetanide: potent new “loop” diuretic. Br Med J. 1972; 1:211-3.

53. Maronde RF, Quinn M. Double blind comparison of furosemide and bumetanide. Clin Pharmacol Ther. 1977; 21:110.

54. Berg KJ, Tromsdal A, Wideroe TE. Diuretic action of bumetanide in advanced chronic renal insufficiency. Eur J Clin Pharmacol. 1976; 9:265-75.

55. Whelton A. Long-term bumetanide treatment of renal edema: comparison with furosemide. J Clin Pharmacol. 1981; 21:591-8.

56. White MG. The effect of intravenous bumetanide in man with normal and low renal function. J Clin Pharmacol. 1981; 21:581-5.

57. Hutcheon DE, Pocelinko R, Duchin KL. Bumetanide in the treatment of hypertension. In: Scriabine A, Sweet CS, eds. New antihypertensive drugs. Proceedings of the AN Richards Symposium. Volume 2. New York: Spectrum Publications; 1976:323-36.

58. Berg KJ. Acute acetylsalicylic acid poisoning: treatment with forced alkaline diuresis and diuretics. Eur J Clin Pharmacol. 1977; 12:111-6.

59. Hayes AH, Shiroff RA, Limjucolz A et al. Effect of bumetanide on the renal excretion of digoxin. Clin Pharmacol Ther. 1979; 25:228.

60. Brater C, Chennavasin P, Beck JM et al. Indomethacin and the response to bumetanide. Clin Pharmacol Ther. 1980; 27:421-5.

61. Kaufman J, Hamburger R, Matheson J et al. Bumetanide-induced diuresis and natriuresis: effect of prostaglandin synthetase inhibition. J Clin Pharmacol. 1981; 21:663-7.

62. Brater DC, Fox WR, Chennavasin P. Interaction studies with bumetanide and furosemide: effects of probenecid and of indomethacin on response to bumetanide in man. J Clin Pharmacol. 1981; 21:647-53.

63. Velasquez MT, Wan SH, Barr JW et al. Effect of probenecid on the natriuresis and renin release induced by bumetanide in man. J Clin Pharmacol. 1981; 21:657-62.

64. Brummett RE, Bendrick T, Himes D. Comparative ototoxicity of bumetanide and furosemide when used in combination with kanamycin. J Clin Pharmacol. 1981; 21:628-36.

65. Nilsson CM, Horton ES, Robinson DS. The effect of furosemide and bumetanide on warfarin metabolism and anticoagulant response. J Clin Pharmacol. 1978; 18:91-4.

66. Nipper H, Kirby S, Iber FL. The effect of bumetanide on the serum disappearance of warfarin sodium. J Clin Pharmacol. 1981; 21:654-6.

67. Hunter KR, Underwood PN. Evaluation of once-daily versus twice-daily bumetanide in heart failure. Postgrad Med J. 1975; 21(Suppl. 6):91-5.

68. Duchin KL, Hutcheon DE. Comparison of bumetanide and hydrochlorothiazide on renal potassium and hydrogen ion excretion. J Clin Pharmacol. 1977; 17:453-60.

69. McCormack P. Bumetanide in renal failure. Lancet. 1976; 2:104.

70. Lemieux G, Beauchemin M, Gougoux A et al. Treatment of nephrotic edema with bumetanide. Can Med Assoc J. 1981; 125:1111-7.

71. Olsen UB. Indomethacin inhibition of bumetanide diuresis in dogs. Acta Pharmacol Toxicol (Copenh). 1975; 37:65-78.

72. Mudge GH. Drugs affecting renal function and electrolyte metabolism. In: Gilman AG, Goodman L, Gilman A, eds. Goodman and Gilman’s the pharmacological basis of therapeutics. 6th ed. New York: Macmillan Publishing Company; 1980:903-7.

73. Abrams J. Intramuscular bumetanide and furosemide in congestive heart failure. J Clin Pharmacol. 1981; 21:673-9.

74. Poisindex. Rumack BH, ed. Overview—salicylates. Englewood, CO: Micromedex Inc.; 1982 Aug 31.

75. USP DI. Vol. 1: 1984 Drug information for the health care provider. Rockville, MD: The United States Pharmacopeial Convention, Inc.; 1983:262-3.

76. Hoechst-Roussel Pharmaceuticals Inc. Lasix prescribing information. In: Huff BB, ed. Physicians’ desk reference. 38th ed. Oradell, NJ: Medical Economics Company Inc.; 1984:1003-5.

77. Petersdorf RG, Adams RD, Braunwald E et al, eds. Harrison’s principles of internal medicine. 10th ed. New York: McGraw-Hill Book Co.; 1983:234-5, 1359.

78. Watkins J, Abbott EC, Hensky CN et al. Attenuation of hypotensive effect of propranolol and thiazide diuretics by indomethacin. Br Med J. 1980; 281:702-5.

79. Hansten PD. Drug interactions. 4th ed. Philadelphia: Lea & Febiger; 1979:137, 194, 203, 204.

80. Koch-Weser J. Drug interactions in cardiovascular therapy. Am Heart J. 1975; 90:93-116.

81. Mulhall B. (Roche Laboratories, Nutley, NJ): Personal communication; 1984 May 30.

82. Reviewers’ comments (personal observations); 1984 May, Jun.

83. Rowe JW, Tobin JD, Rosa RM et al. Effect of experimental potassium deficiency on glucose and insulin metabolism. Metabolism. 1980; 29:498-502.

84. Helderman JH, Elahi D, Andersen DK et al. Prevention of the glucose intolerance of thiazide diuretics by maintenance of body potassium. Diabetes. 1983; 32:106-11.

85. Miller RD, Sohn YJ, Matteo RS. Enhancement of d-tubocurarine neuromuscular blockade by diuretics in man. Anesthesiology. 1976; 45:442-45.

86. Dollery CT, Parry EHO, Young DS. Diuretic and hypotensive properties of ethacrynic acid: a comparison with hydrochlorothiazide. Lancet. 1964; 1:947-52.

87. Puschett JB. Sites and mechanisms of action of diuretics in the kidney. J Clin Pharmacol. 1981; 21:564-74.

88. Dixon WR, Young RL, Holazo A et al. Bumetanide: radioimmunoassay and pharmacokinetic profile in humans. J Pharm Sci. 1976; 65:701-4.

89. Burg MB. Thick ascending limb of Henle’s loop. Kidney Int. 1982; 22:454-64.

90. McNabb WR, Noormohamed FH, Brooks BA et al. Renal actions of piretanide and three other “loop” diuretics. Clin Pharmacol Ther. 1984; 35:328-37.

91. Pentikainen PJ, Pasternack A, Lampainen E et al. Bumetanide kinetics in renal failure. Clin Pharmacol Ther. 1985; 37:582-8.

92. Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. The 1984 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med. 1984; 144:1045-57.

93. Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. The 1980 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med. 1980; 140:1280-5.

94. 1988 Joint National Committee. The 1988 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med. 1988; 148:36-69.

95. The United States Pharmacopeia, 22nd rev, and The national formulary, 17th ed. Rockville, MD: The United States Pharmacopeial Convention, Inc; 1990:192.

96. Lardinois CK, Neuman SL. The effects of antihypertensive agents on serum lipids and lipoproteins. Arch Intern Med. 1988; 148:1280-8.

97. Holland OB, Pool PE. Metabolic changes with antihypertensive therapy of the salt-sensitive patient. Am J Cardiol. 1988; 61:53-9H.

98. Weinberger MH. Diuretics and their side effects: dilemma in the treatment of hypertension. Hypertension. 1988; 11(Suppl II):II-16-20.

99. Ames R. Effects of diuretic drugs on the lipid profile. Drugs. 1988; 36(Suppl 2):33-40.

100. Lasser NL, Grandits G, Caggiula AW et al. Effects of antihypertensive therapy on plasma lipids and lipoproteins in the Multiple Risk Factor Intervention Trial. Am J Med. 1984; 76(Suppl 2A):52-66.

101. Lau HSH, Hyneck ML, Berardi RR et al. Kinetics, dynamics, and bioavailability of bumetanide in healthy subjects and patients with chronic renal failure. Clin Pharmacol Ther. 1986; 39:635-45.

102. Bloomgarden ZT, Ginsberg-Fellner F, Rayfield EJ et al. Elevated hemoglobin A1c and low-density lipoprotein cholesterol levels in thiazide-treated diabetic patients. Am J Med. 1984; 77:823-7.

103. Gluck Z, Baumgartner G, Weidmann P et al. Increased ratio between serum beta- and alpha-lipoproteins during diuretic therapy: an adverse effect? Clin Sci Mol Med Suppl. 1978; 4:325-8s.

104. Ames RP, Hill P. Antihypertensive therapy and the risk of coronary heart disease. J Cardiovasc Pharmacol. 1982; 4(Suppl 2):S206-12.

105. Ames RP, Hill P. Improvement of glucose tolerance and lowering of glycohemoglobin and serum lipid concentrations after discontinuance of antihypertensive drug treatment. Circulation. 1982; 65:899-904.

106. Perola P, Lehto H, Lammintausta R et al. Metabolic effects of furosemide and the combination of furosemide and triamterene. Curr Ther Res. 1985; 37:545-53.

107. Weinberger MH. Antihypertensive therapy and lipids: evidence, mechanisms, and implications. Arch Intern Med. 1985; 145:1102-5.

108. Weidmann P, Gerber A. Effects of treatment on serum lipoproteins. J Cardiovasc Pharmacol. 1984; (6 Suppl 1):S260-8.

109. Weidmann P, Gerber A, Mordasini R. Effects of antihypertensive therapy on serum lipoproteins. Hypertension. 1983; 5(5 Part 2):III-120-31.

111. Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. The fifth report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC V). Arch Intern Med. 1993; 153:154-83.

113. Kaplan NM. Choice of initial therapy for hypertension. JAMA. 1996; 275:1577-80.

114. Psaty BM, Smith NL, Siscovich DS et al. Health outcomes associated with antihypertensive therapies used as first-line agents: a systematic review and meta-analysis. JAMA. 1997; 277:739-45.

115. Whelton PK, Appel LJ, Espeland MA et al. for the TONE Collaborative Research Group. Sodium reduction and weight loss in the treatment of hypertension in older persons: a randomized controlled trial of nonpharmacologic interventions in the elderly (TONE). JAMA. 1998; 279:839-46.

116. Anon. Consensus recommendations for the management of chronic heart failure. On behalf of the membership of the advisory council to improve outcomes nationwide in heart failure. Part II. Management of heart failure: approaches to the prevention of heart failure. Am J Cardiol. 1999; 83:9-38A.

117. The Captopril-Digoxin Multicenter Research Group. Comparative effects of therapy with captopril and digoxin in patients with mild to moderate heart failure. JAMA. 1988; 259:539-44.

118. Richardson A, Bayliss J, Scriven AJ et al. Double-blind comparison of captopril alone against frusemide plus amiloride in mild heart failure. Lancet. 1987; 2:709-11.

119. Sherman LG, Liang CS, Baumgardner S et al. Piretanide, a potent diuretic with potassium-sparing properties, for the treatment of congestive heart failure. Clin Pharmacol Ther. 1986; 40:587-94.

120. Patterson JH, Adams KF Jr, Applefeld MM et al. Oral torsemide in patients with chronic congestive heart failure: effects on body weight, edema, and electrolyte excretion. Pharmacotherapy. 1994; 14:514-21.

121. Wilson JR, Reichek N, Dunkman WB et al. Effect of diuresis on the performance of the failing left ventricle in man. Am J Med. 1981;70:234-9.

122. Parker JO. The effects of oral ibopamine in patients with mild heart failure--a double blind placebo controlled comparison to furosemide. Int J Cardiol. 1993; 40:221-7.

123. Izzo JL, Levy D, Black HR. Importance of systolic blood pressure in older Americans. Hypertension. 2000; 35:1021-4.

124. Frohlich ED. Recognition of systolic hypertension for hypertension. Hypertension. 2000; 35:1019-20.

125. Bakris GL, Williams M, Dworkin L et al. Preserving renal function in adults with hypertension and diabetes: a consensus approach. Am J Kidney Dis. 2000; 36:646-61.

126. Associated Press (American Diabetes Association). Diabetics urged: drop blood pressure. Chicago, IL; 2000 Aug 29. Press Release from web site.

127. Appel LJ. The verdict from ALLHAT—thiazide diuretics are the preferred initial therapy for hypertension. JAMA. 2002; 288:3039-42.

128. The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA. 2002; 288:2981-97.

132. The Guidelines Subcommittee of the WHO/ISH Mild Hypertension Liaison Committee. 1999 guidelines for the management of hypertension. J Hypertension. 1999; 17:392-403.

501. James PA, Oparil S, Carter BL et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014; 311:507-20.

502. Mancia G, Fagard R, Narkiewicz K et al. 2013 ESH/ESC Guidelines for the management of arterial hypertension: the Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens. 2013; 31:1281-357.

503. Go AS, Bauman MA, Coleman King SM et al. An effective approach to high blood pressure control: a science advisory from the American Heart Association, the American College of Cardiology, and the Centers for Disease Control and Prevention. Hypertension. 2014; 63:878-85.

504. Weber MA, Schiffrin EL, White WB et al. Clinical practice guidelines for the management of hypertension in the community: a statement by the American Society of Hypertension and the International Society of Hypertension. J Clin Hypertens (Greenwich). 2014; 16:14-26.

505. Wright JT, Fine LJ, Lackland DT et al. Evidence supporting a systolic blood pressure goal of less than 150 mm Hg in patients aged 60 years or older: the minority view. Ann Intern Med. 2014; 160:499-503.

506. Mitka M. Groups spar over new hypertension guidelines. JAMA. 2014; 311:663-4.

507. Peterson ED, Gaziano JM, Greenland P. Recommendations for treating hypertension: what are the right goals and purposes?. JAMA. 2014; 311:474-6.

508. Bauchner H, Fontanarosa PB, Golub RM. Updated guidelines for management of high blood pressure: recommendations, review, and responsibility. JAMA. 2014; 311:477-8.

515. Thomas G, Shishehbor M, Brill D et al. New hypertension guidelines: one size fits most?. Cleve Clin J Med. 2014; 81:178-88.

523. Fihn SD, Gardin JM, Abrams J et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2012; 126:e354-471.

524. WRITING COMMITTEE MEMBERS, Yancy CW, Jessup M et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2013; 128:e240-327.

526. Kernan WN, Ovbiagele B, Black HR et al. Guidelines for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2014; 45:2160-2236.

530. Myers MG, Tobe SW. A Canadian perspective on the Eighth Joint National Committee (JNC 8) hypertension guidelines. J Clin Hypertens (Greenwich). 2014; 16:246-8.

536. Kidney Disease: Improving Global Outcomes (KDIGO) Blood Pressure Work Group. KDIGO clinical practice guideline for the management of blood pressure in chronic kidney disease. Kidney Int Suppl. 2012: 2: 337-414.

700. Yancy CW, Jessup M, Bozkurt B et al. 2016 ACC/AHA/HFSA Focused Update on New Pharmacological Therapy for Heart Failure: An Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Circulation. 2016; :.

713. Gupta D, Georgiopoulou VV, Kalogeropoulos AP et al. Dietary sodium intake in heart failure. Circulation. 2012; 126:479-85.

714. Hospira. Dopamine hydrochloride prescribing information. Lake Forest, IL; 2014 Mar.

715. Hospira. Dopamine hydrochloride and 5% dextrose injection prescribing information. Lake Forest, IL; 2014 May.

716. Cicci JD, Reed BN, McNeely EB et al. Acute decompensated heart failure: evolving literature and implications for future practice. Pharmacotherapy. 2014; 34:373-88.

717. Triposkiadis FK, Butler J, Karayannis G et al. Efficacy and safety of high dose versus low dose furosemide with or without dopamine infusion: the Dopamine in Acute Decompensated Heart Failure II (DAD-HF II) trial. Int J Cardiol. 2014;172(1):115-21.

718. Torres-Courchoud I, Chen HH. Is there still a role for low-dose dopamine use in acute heart failure?. Curr Opin Crit Care. 2014; 20:467-71.

719. Houston BA, Kalathiya RJ, Kim DA et al. Volume Overload in Heart Failure: An Evidence-Based Review of Strategies for Treatment and Prevention. Mayo Clin Proc. 2015; 90:1247-61.

720. Chen HH, Anstrom KJ, Givertz MM et al. Low-dose dopamine or low-dose nesiritide in acute heart failure with renal dysfunction: the ROSE acute heart failure randomized trial. JAMA. 2013; 310:2533-43.

723. Hummel SL, Konerman MC. Dietary Sodium Restriction in Heart Failure: A Recommendation Worth its Salt?. JACC Heart Fail. 2016; 4:36-8.

724. Yancy CW. The Uncertainty of Sodium Restriction in Heart Failure: We Can Do Better Than This. JACC Heart Fail. 2016; 4:39-41.

1200. Whelton PK, Carey RM, Aronow WS et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018; 71:el13-e115.

1201. Bakris G, Sorrentino M. Redefining hypertension - assessing the new blood-pressure guidelines. N Engl J Med. 2018; 378:497-499.

1202. Carey RM, Whelton PK, 2017 ACC/AHA Hypertension Guideline Writing Committee. Prevention, detection, evaluation, and management of high blood pressure in adults: synopsis of the 2017 American College of Cardiology/American Heart Association hypertension guideline. Ann Intern Med. 2018; 168:351-358.

1207. Burnier M, Oparil S, Narkiewicz K et al. New 2017 American Heart Association and American College of Cardiology guideline for hypertension in the adults: major paradigm shifts, but will they help to fight against the hypertension disease burden?. Blood Press. 2018; 27:62-65.

1209. Qaseem A, Wilt TJ, Rich R et al. Pharmacologic treatment of hypertension in adults aged 60 years or older to higher versus lower blood pressure targets: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians. Ann Intern Med. 2017; 166:430-437.

1210. SPRINT Research Group, Wright JT, Williamson JD et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015; 373:2103-16.

1216. Taler SJ. Initial treatment of hypertension. N Engl J Med. 2018; 378:636-644.

1220. Cifu AS, Davis AM. Prevention, detection, evaluation, and management of high blood pressure in adults. JAMA. 2017; 318:2132-2134.

1222. Bell KJL, Doust J, Glasziou P. Incremental benefits and harms of the 2017 American College of Cardiology/American Heart Association high blood pressure guideline. JAMA Intern Med. 2018; 178:755-7.

1223. LeFevre M. ACC/AHA hypertension guideline: what is new? what do we do?. Am Fam Physician. 2018; 97(6):372-3.

1224. Brett AS. New hypertension guideline is released. From NEJM Journal Watch website. Accessed 2018 Jun 18.

1229. Ioannidis JPA. Diagnosis and treatment of hypertension in the 2017 ACC/AHA guidelines and in the real world. JAMA. 2018; 319(2):115-6.

a. Roche Laboratories. Bumex (bumetanide) tablets prescribing information. Nutley, NJ; 2003 March.

b. Bedford Laboratories. Bumetanide injection prescribing information. Bedford, OH; 1998 Sept.

HID. Trissel LA. Handbook on injectable drugs. 17th ed. Bethesda, MD: American Society of Health-System Pharmacists; 2013:161-3.

d. AHFS Drug Information 2017. McEvoy GK, ed. Bumetanide. American Society of Health-System Pharmacists; 2017: .