Bumetanide is a loop diuretic used to treat fluid retention (oedema) associated with heart failure, liver disease and kidney disease, including nephrotic syndrome. It is more potent than furosemide (1 mg ≈ 40 mg of furosemide) and acts rapidly. Electrolytes and renal function must be monitored.
Also known as: Burinex
Loop plus potassium-sparing diuretic: risk of electrolyte imbalance.
Spironolactone (potassium-sparing diuretic) and bumetanide (loop diuretic, which excretes potassium) are often used together in heart failure to balance potassium — bumetanide removes K+ and spironolactone retains it. The spironolactone label states that "concomitant administration may lead to hyperkalaemia" and classifies potassium-depleting diuretics as an interaction to monitor; the bumetanide label was not individually analysed, but the net effect depends on renal function and relative doses. In patients with creatinine clearance > 50 mL/min, the balance is generally favourable; in CKD (clearance < 30 mL/min), the risk of hyperkalaemia increases. Monitor potassium and creatinine before initiation and 1 week after; adjust doses according to potassium (if K+ < 3,5 increase spironolactone or reduce bumetanide; if K+ > 5,0 reduce spironolactone or increase bumetanide).
Spironolactone + bumetanide: combination used to regulate potassium in HF (loop loses K, spironolactone spares). Balance depends on renal function; monitor K+.
Used together to manage potassium; balance depends on renal function.
Potassium, creatinine, diuresis.
Cramps, arrhythmia or hypotension.
Monitor electrolytes; avoid in advanced renal failure.
DailyMed (FDA) — approved Bumetanide label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=4a9229c8-89ba-423e-8e36-f56bc329ed38 ; approved Spironolactone label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=57d1c333-c229-54aa-e063-6394a90a84ce — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Bumetanide-induced hypokalaemia increases digoxin toxicity.
Bumetanide is a loop diuretic that depletes potassium and magnesium. These electrolytes are critical in digitalis toxicity: hypokalaemia and hypomagnesaemia potentiate the arrhythmogenic effects of digoxin (aggravated Na+/K+-ATPase blockade), even at therapeutic digoxin levels. The risk is higher in elderly patients, in those with reduced renal function or with high diuretic doses. Monitor serum potassium and magnesium (keeping K+ ≥ 4.0 mEq/L), correct deficits, monitor the ECG and consider digoxin level monitoring.
Loop diuretic + digoxin: diuretic-induced hypokalaemia and hypomagnesaemia increase digitalis toxicity. Monitor electrolytes and digoxin levels.
Loop-diuretic potassium depletion sensitizes the myocardium to digoxin.
Potassium, digoxin levels, ECG.
Arrhythmia or bradycardia with nausea.
Monitor potassium and digoxin toxicity signs.
DailyMed (FDA) — approved Bumetanide label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=4a9229c8-89ba-423e-8e36-f56bc329ed38 ; approved Digoxin label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=e61d2108-d871-44c0-b12a-2e61fbb56967 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Liquorice causes pseudoaldosteronism with sodium retention and potassium depletion, opposing the diuretic effect and increasing the risk of hypokalaemia.
Avoid excessive liquorice intake during bumetanide treatment.
EMC-UK (MHRA) — approved Bumetanide SmPC: https://www.medicines.org.uk/emc/product/13372/smpc
Bumetanide is contraindicated in anuria because the diuretic effect depends on adequate renal function.
Do not use in patients with anuria.
EMC-UK (MHRA) — approved Bumetanide SmPC: https://www.medicines.org.uk/emc/product/13372/smpc
Bumetanide is contraindicated in hepatic encephalopathy because potassium depletion may precipitate hepatic coma.
Do not use in patients with hepatic encephalopathy.
EMC-UK (MHRA) — approved Bumetanide SmPC: https://www.medicines.org.uk/emc/product/13372/smpc
Bumetanide crosses the placenta; data in pregnancy are limited and use should only occur if the benefit outweighs the risk.
Avoid as routine diuretic therapy in pregnancy; restrict to clear indications (e.g. pulmonary oedema).
Bumetanide is excreted into breast milk; monitor the infant and consider suppressing lactation at high doses.
Diuretics are not indicated in normal pregnancy; chronic use in women of childbearing age should be reviewed.
EMC-UK (MHRA) — approved Bumetanide SmPC: https://www.medicines.org.uk/emc/product/13372/smpc
Clinical and educational support tool. The information does not replace a medical prescription or the opinion of a qualified healthcare professional.
Loop diuretic with rapid onset and short duration of action; 1 mg of bumetanide has a diuretic potency equivalent to approximately 40 mg of furosemide. Indicated for oedema associated with congestive heart failure, hepatic and renal disease, including the nephrotic syndrome. Onset of oral diuresis occurs within 30-60 minutes, peak activity between 1-2 hours and diuresis is largely complete within 4 hours (4-6 h with higher doses).
Inhibits sodium reabsorption in the ascending limb of the loop of Henle (marked reduction of free-water clearance during hydration and of tubular free-water reabsorption during hydropenia); also blocks chloride reabsorption (somewhat more chloruretic than natriuretic) and increases potassium excretion in a dose-related fashion. May have an additional action in the proximal tubule (phosphaturia); does not inhibit carbonic anhydrase nor have relevant distal tubule action. Decreases uric acid excretion and raises serum uric acid.
Almost equal diuretic response occurs after oral and parenteral administration. Rapid oral absorption, with onset of diuresis within 30-60 minutes and peak activity between 1-2 hours after dosing. In the elderly (65-73 years) total clearance is lower (1.8 vs 2.9 mL/min/kg) and peak concentrations higher (16.9 vs 10.3 ng/mL) compared with younger adults.
Rapidly eliminated; a carbon-14 labelled bumetanide study showed 81% of radioactivity excreted in urine, 45% as unchanged drug. The urinary and biliary metabolites identified are formed by oxidation of the N-butyl side chain. Biliary excretion amounts to only 2% of the dose. Plasma protein binding 94-96%.
Elimination half-life of 1 to 1.5 hours in adults with normal renal function. In neonates elimination is considerably slower (apparent half-life about 6 hours at birth, ~2.4 hours at 1 month; 2.5 h <2 months, 1.5 h 2-6 months). Potential for ototoxicity (5-6 times more potent than furosemide in animal studies).
Medicines from the same therapeutic group (ATC classification) or the same pharmacological class.
