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Furosemide !

The most used loop diuretic: it removes fluid quickly in heart failure, pulmonary oedema and other oedemas, and lowers potassium.

Updated 2026-11-01

  • Class: Loop diuretics
  • Transporter: Na⁺-K⁺-2Cl⁻ cotransporter (NKCC2) of the loop of Henle
  • ATC code: C03CA01
  • WHO Model List of Essential Medicines

Also called: Frusemide

The figure shows furosemide bound to human NKCC1, the closely related cotransporter found outside the kidney; NKCC2, the renal target, belongs to the same family and binds loop diuretics in the same way.

Target in 3D: Na⁺-K⁺-2Cl⁻ cotransporter (NKCC2) of the loop of Henle. PDB structure 9C0E (RCSB PDB, public domain). View the structure at RCSB PDB

Mechanism of action

Furosemide is secreted into the tubule by the proximal tubule's organic acid transporters and, from the lumen, blocks NKCC2 in the thick ascending limb. Sodium, potassium and chloride are not reabsorbed, the medullary concentration gradient falls and a large volume of urine follows. Loss of the lumen-positive voltage also increases calcium and magnesium excretion. Given IV it also dilates veins, which helps in pulmonary oedema.

  1. Furosemide reaches the tubule lumen by secretion
  2. It blocks NKCC2 in the thick ascending limb
  3. Na⁺, K⁺ and Cl⁻ stay in the urine and water follows
  4. Rapid diuresis; more K⁺, Mg²⁺ and Ca²⁺ are lost

Pharmacokinetics

Absorption
Absorbed by mouth, but only partly and variably; the IV route gives a faster, larger effect
Distribution
Highly bound to albumin; low albumin (nephrotic syndrome) weakens its effect
Metabolism
Partly conjugated to a glucuronide
Elimination
Mostly unchanged in the urine; it accumulates in kidney failure
Half-life
About 2 hours
Onset and duration
IV: diuresis within about 5 minutes, peak within half an hour, lasting about 2 hours

Indications

Adverse effects

Common

  • Excessive diuresis, dehydration and low blood pressure on standing
  • Hypokalaemia, hypomagnesaemia and hypocalcaemia
  • Hyponatraemia and metabolic alkalosis
  • High uric acid and gout
  • Higher blood glucose
  • Photosensitivity

Contraindications

  • Anuria
  • Hypersensitivity to furosemide (possible cross-reaction in sulfonamide allergy)
  • Hepatic coma or severe electrolyte depletion until corrected

Key interactions

Aminoglycosides, cisplatin or etacrynic acid
More ototoxicity
Lithium
Less lithium clearance and risk of lithium toxicity
Digoxin
Low potassium and magnesium increase digoxin toxicity
NSAIDs (e.g. indometacin)
Weaker diuretic and antihypertensive effect, and risk of kidney injury
ACE inhibitors or ARBs
Marked hypotension and worsening kidney function

What is monitored

  • Potassium, sodium, magnesium and calcium
  • Creatinine and urea
  • Weight, fluid balance and urine output
  • Blood pressure, including on standing
  • Hearing at high IV doses
  • Blood glucose and uric acid

Administration and safety

  • Given by mouth, IV or IM; the IV dose is injected slowly or infused, because fast injection raises the risk of ototoxicity.
  • Protect the solution from light; do not use it if discoloured.
  • It is alkaline and can precipitate when mixed with acidic solutions: check compatibility before adding it to a line.
  • Give earlier in the day to avoid night-time urination.

Nursing care

  • Before giving: blood pressure, potassium and kidney function; hold and report if potassium is low or the patient is hypotensive.
  • Daily weight at the same time, intake and output, and signs of oedema or dehydration.
  • Watch for low potassium (weakness, cramps, arrhythmias) and digoxin toxicity in patients on digoxin.
  • Ask about tinnitus or hearing loss, especially with IV use or aminoglycosides.
  • Teach: rise slowly to avoid dizziness, protect the skin from the sun, report thirst, cramps or reduced urine.

Pregnancy and breastfeeding

Not a usual treatment in pregnancy; it crosses the placenta and fetal growth is monitored if it is used.

Test yourself

Think of the answer, then tap the question to see it.

Where and on what does furosemide act?

On the Na⁺-K⁺-2Cl⁻ cotransporter (NKCC2) in the thick ascending limb of the loop of Henle, reaching it from the tubule lumen.

Can you name four electrolyte changes furosemide can cause?

Hypokalaemia, hypomagnesaemia, hypocalcaemia and hyponatraemia, plus hypochloraemic metabolic alkalosis.

Which drug combination increases furosemide's ototoxicity?

Aminoglycosides, cisplatin or etacrynic acid, especially with fast IV injection or kidney failure.

Why do NSAIDs reduce the effect of furosemide?

They block prostaglandin synthesis in the kidney, which reduces renal blood flow and the natriuretic response to the diuretic.

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Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: DailyMed - FUROSEMIDE injection, solution (DailyMed (U.S. National Library of Medicine), 2026); Furosemide: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2025); ATCDDD - ATC/DDD Index (WHO Collaborating Centre for Drug Statistics Methodology, 2026); eEML - Electronic Essential Medicines List (World Health Organization, 2025).

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Representative model, for educational purposes only.