Loop diuretics
ATC code: C03CA01 (Furosemide)
Brand names
Lasix
Inhibits the Na+/K+/2Cl– cotransporter (NKCC2) in the thick ascending limb of the loop of Henle – produces potent natriuresis and diuresis up to 25 % of filtrate. Drug of choice for volume overload (acute pulmonary edema, decompensated HF, ascites, edema). Rapid onset after IV administration (5 minutes). Accompanied by loss of potassium, magnesium and calcium, with risk of metabolic alkalosis, hyperuricemia, and ototoxicity from rapid IV bolus of high doses.
First line
First-line in acute decompensated HF with pulmonary edema per HF 2021. IV bolus 20–40 mg (or twice the chronic oral daily dose in pre-treated patients). With inadequate response, continuous infusion. Goal: sustained 3–5 L diuresis in the first 24–48 hours and relief of venous congestion. Monitor BP, potassium, creatinine, urine output.
First line
In symptomatic HF with congestion, first-line for symptom control alongside the four pillars of HF 2021 (ACEi/ARNI, beta-blocker, MRA, SGLT2i). Start 20–40 mg orally once or twice daily, titrate to symptoms and weight. Diuretics do not reduce mortality in HF but improve dyspnea, edema, and reduce hospitalizations. Use the lowest effective dose.
Starting dose in HF is 20-40 mg orally once daily, titrated as needed. For acute decompensated HF, intravenous boluses or infusion are used. Dose is adjusted by weight and diuresis.
First line
Loop diuretics are the cornerstone of symptomatic therapy for edematous syndromes in nephrotic syndrome and CKD per KDIGO. In severe hypoalbuminemia, combination with albumin infusion may be required to expand intravascular volume and deliver the drug to its site of action. In eGFR below 30, higher doses (80–160 mg or more) are needed.
Not recommended
For ordinary hypertension, furosemide is rarely prescribed and not recommended as a first choice. 2024, 2017, and NG136 prefer thiazide-like diuretics (indapamide, chlorthalidone) because of a smoother antihypertensive effect and less potassium loss. Furosemide is used in hypertensive patients with marked HF or impaired renal function (eGFR < 30).
Not recommended
Furosemide is sometimes taken 'after a drinking episode' to reduce puffiness. In reality a hangover involves dehydration, not fluid overload – a diuretic worsens the state. Evidence-based measures are water, salt, and simple food. Combining furosemide with alcohol raises hypotension, electrolyte disturbance, and syncope risk.
Not recommended
Self-medication with furosemide for «morning puffiness», «edema from fatigue», and similar complaints without an established clinical diagnosis is unsafe and unsupported by guidelines. Regular use without an indication causes hypokalemia, hyponatremia, dehydration, rebound fluid retention on withdrawal, and diuretic-associated nephropathy. Edema warrants a differential workup: cardiac, renal, hepatic, venous, lymphatic, or drug-induced. Diuretics are started after a cause is established.
Not recommended
Furosemide is sometimes used for 'rapid weight loss' – the effect is fluid loss, not fat loss. This is clinically dangerous: dehydration, electrolyte disturbance (hypokalaemia, hyponatraemia), acute kidney injury, and hypotension. International obesity guidelines ( NG189, //TOS) do not include diuretics. Bodybuilders use furosemide for pre-contest 'cutting' – a practice associated with arrhythmia deaths.
10 pairs found. Sorted from critical to minor.
Mechanism
Dual mechanism. First, aspirin competes with furosemide for tubular organic-anion secretion in the proximal tubule – delivery of furosemide to the luminal side of the loop of Henle falls. The effect is pronounced at high aspirin doses. Second, inhibition of renal prostaglandin synthesis reduces preglomerular vasodilation and natriuresis. At cardiovascular aspirin doses of 75–100 mg, both mechanisms are clinically minor. At analgesic and antipyretic doses of 500–1000 mg and above, the effect becomes clinically obvious – HF and ascites patients may lose diuretic efficacy and develop worsening edema.
Management
Antiplatelet aspirin doses of 75–100 mg are compatible with furosemide. Avoid analgesic and antipyretic doses of 500–1000 mg in HF and ascites – replace with paracetamol. If an NSAID is essential, use the shortest possible course, monitor body weight daily, and check creatinine and potassium at 5–7 days. For worsening edema, temporarily increase the furosemide dose or add a thiazide (sequential nephron blockade).
Sources
Mechanism
Furosemide causes potassium and magnesium loss. Hypokalemia increases cardiomyocyte sensitivity to digoxin – digitalis arrhythmia (atrial tachycardia with AV block, ventricular bigeminy) can develop even at therapeutic concentrations.
Management
Keep potassium above 4.0 mmol/L and magnesium in the upper-normal range. Check electrolytes every 1–3 months on stable therapy, more often when adjusting furosemide. For hypokalemia, use potassium supplements or potassium-sparing diuretics (spironolactone).
Sources
Mechanism
In patients with activated RAAS (significant hypovolemia from aggressive diuresis, severe HF), the first ACE-inhibitor dose can cause an abrupt BP drop with syncope and acute kidney injury. With chronic use, the combination provides synergistic antihypertensive effect.
Management
Before starting an ACE inhibitor, assess volume status and, where possible, hold or reduce furosemide for 24–48 hours. Begin enalapril at the lowest dose (2.5 mg) at night while the patient is recumbent. Check BP, creatinine, and potassium at 3–7 days.
Sources
Mechanism
Аддитивная ототоксичность и нефротоксичность. Описаны случаи необратимой сенсоневральной тугоухости.
Management
Избегать у пожилых и при нарушении функции почек. При необходимости – аудиометрия исходно, контроль креатинина каждые 2–3 дня.
Mechanism
Фуросемид и тиазидные диуретики снижают почечный клиренс лития, концентрация в плазме растет на 25–40%.
Management
Контроль лития через 5–7 дней после старта диуретика, далее каждый месяц. Альтернатива – петлевые диуретики с осторожностью.
Mechanism
Same as the ACE-inhibitor/furosemide pair: in a hypovolemic patient the first sartan dose can cause an abrupt BP drop and acute kidney injury. Chronic combination provides synergistic BP reduction.
Management
Assess volume status before starting losartan. Start at 25–50 mg at night. Check BP, creatinine, and potassium at 3–7 days. In older patients, start at 25 mg.
Sources
Mechanism
Furosemide causes hypokalemia and hypomagnesemia – increasing myocardial sensitivity to amiodarone's QT-prolonging effect. Risk of torsades de pointes.
Management
Keep potassium above 4.0 mmol/L and magnesium in the upper-normal range. Obtain an ECG with QT measurement at baseline, at 1–2 weeks, and after each amiodarone dose change.
Sources
Mechanism
Sequential nephron blockade: furosemide acts in the loop of Henle, the thiazide in the distal tubule. Additive diuresis in furosemide-resistant HF. Risk of severe dehydration, hypokalemia, hyponatremia, hypomagnesemia, and prerenal azotemia.
Management
Use short term (3–7 days) in patients with resistant HF. Monitor electrolytes, creatinine, and body weight daily in inpatients. Supplement with potassium and/or add spironolactone.
Sources
Mechanism
Both drugs can cause hyponatremia (furosemide via natriuresis, sertraline via an SIADH-like mechanism). In patients over 75, the rate of clinically significant hyponatremia (Na+ < 130 mmol/L) rises with the combination.
Management
Check sodium at baseline, at 2 and 4 weeks after sertraline initiation, then every 3–6 months. For Na+ < 130 mmol/L, reassess therapy.
Sources
Mechanism
Opposing effects on potassium: furosemide depletes potassium, spironolactone retains it. A target combination in HF and resistant hypertension. The potassium balance depends on the dose ratio and renal function – in CKD and diabetes, spironolactone dominates and hyperkalemia risk rises.
Management
Check potassium and creatinine 3–7 days after initiation or dose change, then every 1–3 months. Target potassium is 4.0–5.0 mmol/L. If K+ > 5.5 mmol/L, reduce the spironolactone dose.
Sources
FDA categories were retired in 2015 (historically C). Diuretics are not used routinely in pregnancy — they may reduce uteroplacental flow and cause fetal electrolyte disturbance. Use is justified in cardiogenic pulmonary edema and maternal HF under specialist supervision.
Excreted in breast milk in small amounts. May suppress lactation. Per LactMed, use only when necessary and monitor the infant.
furosemide is evaluated for the following indications with varying evidence strength: Edema in heart failure (evidence tier A), Acute pulmonary edema (evidence tier A), Edema in nephrotic syndrome (evidence tier A). See the full indication matrix with dosing and citations above on this page.
Common side effects of furosemide (≥ 1 in 100): Hypokalemia, hyponatremia, hypochloremic alkalosis, Hyperuricemia (gout flare risk), Orthostatic hypotension, Dehydration, rising creatinine, Hearing loss with rapid high-dose IV administration. See the Safety section for uncommon and serious reactions.
FDA categories were retired in 2015 (historically C). Diuretics are not used routinely in pregnancy — they may reduce uteroplacental flow and cause fetal electrolyte disturbance. Use is justified in cardiogenic pulmonary edema and maternal HF under specialist supervision.
Excreted in breast milk in small amounts. May suppress lactation. Per LactMed, use only when necessary and monitor the infant.
furosemide is contraindicated in: Anuria; Severe electrolyte imbalance (hypokalemia, hyponatremia) until corrected; Hepatic coma and pre-coma; Dehydration; Hypersensitivity to sulfonamides. Full list in the Safety section.
mild morning puffiness in healthy people is physiological — a diuretic neither treats it nor is it safe to use.
a single dose removes 1–2 L of fluid that returns within 24 hours. No sustained fat loss occurs. Chronic self-use leads to electrolyte disturbances and nephropathy.
furosemide is on the WADA prohibited list — masks other drugs in doping tests and rapidly reduces weight before weigh-ins in weight-class sports. Non-medical use violates sport rules.