Furosemide


Article Author:
Tahir Khan
Roshan Patel


Article Editor:
Abdul Siddiqui


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
9/16/2019 7:19:58 PM

Indications

The Food and Drug Administration (FDA) has approved the use of furosemide in the treatment of conditions with volume overload and edema secondary to congestive heart failure exacerbation, liver failure, or renal failure including the nephrotic syndrome.  

Patients with acutely decompensated heart failure (ADHF) with volume overload who have not received diuretics previously, the initial dose of furosemide should be 20 to 40 mg intravenously, and later, titrate the furosemide dose according to the clinical response of the patients. However, those patients with ADHF with a normal kidney function who are on chronic diuretic therapy, the initial dose of furosemide can be equivalent to or greater than the total oral maintenance dose of furosemide patient takes per day. Subsequently, the diuretic dose adjustments are according to the clinical response of the patient. Nevertheless, the starting with higher doses of furosemide, that is, at a dose of 2.5 times the total daily oral dose of furosemide per day, has shown a significant trend toward a rapid improvement in the global assessment of patients’ symptoms.[1]

Although the FDA approved the use of loop diuretics alone or in combination with other anti-hypertensive medications as an alternative to thiazide diuretics to treat hypertension. However, the clinical guidelines panel report of Eighth Joint National Committee (JNC-8) published in 2014 and the American College of Cardiology/American Heart Association (ACC/AHA) Task Force Panel Guidelines on hypertension treatment published in 2017 do not recommend the use of loop diuretic as a first-line medication to treat hypertension.[2][3] Nevertheless, Furosemide can be a second-line agent in heart failure patients with symptoms, and in patients with advanced kidney disease with estimated glomerular filtration rate, less than 30 ml per minute the loop diuretics (furosemide) are preferred over thiazide diuretics to treat hypertension.[4] 

In patients with liver cirrhosis and ascites, diuretic therapy is recommended, accompanied by dietary sodium restriction. The recommended diuretics are a combination of spironolactone and furosemide, starting at a ratio of 100 mg of spironolactone and 40 mg of furosemide.[5] They are titrated up to the dose of diuretics in an increment of the same ratio until achieving the adequate response to diuretic therapy or reaching a maximum dose of 400 mg of spironolactone plus 160 mg of furosemide.[5] However, in cases of intolerance to diuretics secondary to borderline blood pressure, the diuretics can be started at relatively lower doses of 50 mg of spironolactone with 20 mg of furosemide.

Mechanism of Action

Furosemide inhibits tubular reabsorption of sodium and chloride in the proximal and distal tubules, as well as in the thick ascending loop of Henle by inhibiting sodium-chloride cotransport system resulting in excessive excretion of water along with sodium, chloride, magnesium, and calcium.[6]

Administration

Furosemide is available in the oral and intravenous formulations. The administration of oral furosemide can be in the form of tablets or oral solution. Intravenous furosemide is twice as potent as oral furosemide.

In patients with the normal renal function, the oral dose equivalence of furosemide relative to other oral diuretics is as follows[7]:

  • 40 mg of furosemide = 20 mg of torsemide = 1 mg of bumetanide
  • Furosemide oral tablet formulations are available in 20 mg, 40 mg, and 80 mg dosages.
  • Furosemide oral solution is available as 10 mg of furosemide per ml formulation or 8 mg per ml, i.e., 40 mg furosemide per 5 ml of solution.

Furosemide glucuronide is a major biotransformation active product of furosemide having an active diuretic effect.[8] In healthy individuals, greater than 95% of furosemide is bound to plasma protein, mainly albumin. Only 2.3% to 4.1% of furosemide is existent in an unbound form in therapeutic concentrations. 

The terminal half-life of furosemide is approximately 2 hours, and the total time of therapeutic effect is 6 to 8 hours. However, the half-life of furosemide will prolong in patients with chronic renal disease.

The onset of action of furosemide is usually within the first hour of oral furosemide intake, and it takes first 1 to 2 hours to achieve a peak effect. The mean bioavailability of oral furosemide is 51% compared with the bioavailability of intravenously administered furosemide.[9] Although more furosemide gets excreted in the urine after IV administration, there is no difference in the amount of unchanged furosemide excretion in urine between the two formulations. Furosemide achieves an early and high serum peak concentration and a higher peak excretion rate after intravenous administration. Oral and sublingual administration of furosemide achieves a peak concentration slower as compared with the iv route. Although furosemide is more avidly absorbed with a bioavailability of 59% via sublingual route as compared with the oral route of administration, i.e., 47%,  the half-life and time to peak concentration were not different between the oral and sublingual route of drug delivery. Also, urinary excretion rate of furosemide and sodium, and cumulative urine excretion rate was not different between the oral and sublingual administration of furosemide.[10] Moreover, peak plasma concentration increases proportionately with the increasing doses of furosemide, but time-to-peak plasma level does not vary corresponding to different doses. Average bioavailability of furosemide is approximately 50% with a range of 10 to 100%. Bioavailability of furosemide is variable and also relatively lesser than that of torsemide in patients with compensated congestive heart failure.[11][12] The furosemide absorption is slower than normal in patients with edema, particularly in patients with decompensated heart failure; however, the amount of loop diuretic absorbed is normal.[13] 

Breaking phenomenon and ceiling effect: Normally, when an individual receives furosemide either orally or intravenously, it increases sodium excretion in urine. In a patient with extracellular volume expansion who has never had exposure to furosemide, the first dose of the drug causes significant sodium excretion and diuresis within the first 3 to 6 hours. After that effect of furosemide weans off, the kidney starts retaining sodium and chloride; this is called "post-diuretic sodium retention." It is imperative to repeat the furosemide dose at 6 to 8-hour intervals to avoid post diuretic sodium retention and achieve significant diuresis. When furosemide is prescribed chronically, the patient's weight loss correlates with urine volume. A discrepancy in weight loss and diuresis indicates excessive sodium intake by the patient, which can be detected by 24-hour urine sodium collection.

In normal person and patient with extracellular fluid (ECF) expansion, there is a linear relationship between ECF expansion and natriuresis when receiving furosemide; this means that the patient will have higher natriuresis and urine output if ECF volume expands as compared to a person with normal ECF volume. As the use of furosemide becomes chronic in a patient, ECF volume shrinks, and the amount of natriuresis also goes down. At that point amount of natriuresis is equal to sodium intake; this is called "braking phenomenon." This phenomenon is adaptive when it occurs at low ECF volume. But in chronic heart failure patients with persistent ECF volume expansion, this phenomenon is maladaptive. Natriuresis is lower even when ECF volume becomes expanded. The reason for these maladaptive changes is remodeling in the distal nephron. There are hypertrophy and hyperplasia of distal segments of the nephron. These result from increased salt delivery, increased aldosterone, and angiotensin II as well as a change in potassium concentration. As a result of distal segment hypertrophy, sodium transport capacity increases which rivals furosemide's sodium absorption inhibiting capacity at the level of the thick ascending loop of henley. This phenomenon can be overcome by adding thiazide diuretics which blocks sodium absorption in distal segments of the nephron.[14][15]

Adverse Effects

The following are adverse effects associated with furosemide use[16][11]:

  • Hypokalemia
  • Hypomagnesemia
  • Hypocalcemia
  • Hyperglycemia
  • Glycosuria
  • Hyperuricemia
  • Hypertriglyceridemia
  • Increased cholesterol levels
  • Orthostatic hypotension
  • Vasculitis
  • Thrombophlebitis
  • Dizziness
  • Vertigo
  • Headache
  • Paresthesia
  • Hearing impairment
  • Tinnitus
  • Dehydration
  • Muscle cramps
  • Abdominal cramping
  • Anorexia
  • Constipation or diarrhea
  • Pancreatitis
  • Hepatic encephalopathy
  • Anemia
  • Aplastic anemia
  • Eosinophilia
  • Agranulocytosis
  • Hemolytic anemia
  • Interstitial nephritis
  • Renal injury
  • Hypersensitivity reactions
  • Anaphylaxis
  • Skin photosensitivity
  • Bullous pemphigoid
  • Erythema multiforme
  • Exfoliative dermatitis
  • Acute generalized exanthematous pustulosis
  • Stevens-Johnson syndrome
  • Toxic epidermal necrolysis
  • Urticaria
  • Fever

Contraindications

Contraindications to furosemide use include patients with documented allergy to furosemide and patients with anuria.

Monitoring

Caution is necessary with the use of furosemide.

There is a black box warning suggesting the cautious use of furosemide as it is a potent diuretic, can predispose to excessive loss of water and electrolytes resulting in dehydration with electrolyte depletion.

According to Beers Criteria, caution is necessary when administering diuretics to patients 65 years and older to avoid potential adverse effects of inducing hyponatremia by causing or exacerbating syndrome of inappropriate antidiuretic hormone secretion (SIADH); therefore, close monitoring of serum sodium is advisable at initiation or during the dose adjustment in older adults.[17]

Ototoxicity can occur with the use of furosemide, but the following conditions predispose patients to a higher risk of reversible or irreversible hearing impairment[18]:

  • Use of a higher than the recommended dose of furosemide or a fast infusion rate of the drug,
  • Hypoalbuminemic comorbid illnesses
  • The concomitant use of ethacrynic acid, aminoglycosides, or other ototoxic drugs
  • Patients with underlying severe renal impairment

Caution is also necessary for patients with underlying liver disease, especially those with the decompensated liver disease as rapid electrolytes imbalance secondary to furosemide use can precipitate hepatic encephalopathy and hepatic coma. In patients with hepatic coma, the prescriber should delay giving furosemide until improvement in the mental status of the patient.[5]

In patients with advanced renal disease with fluid overload the patients should be closely monitored for oliguria, azotemia and volume status; and if either of oliguria or azotemia develops the furosemide should use should be discontinued to prevent kidney injury.

In patients with primary adrenal insufficiency with hypertension, the use of diuretics to treat hypertension is a practice clinicians should avoid. Alternatively, the dosage of glucocorticoid/mineralocorticoid should be adjusted, and, if needed, other classes of antihypertensive agents may be preferred over diuretics to treat hypertension.[19]

High-risk patients for radiocontrast-induced nephropathy are more predisposed to having a worsened kidney function if furosemide is given before contrast administration as compared to the high-risk patients receiving gentle hydration before contrast exposure.

Patients with a known history of urinary retention due to, for example, benign prostatic hyperplasia, neurogenic bladder with bladder evacuation abnormalities, or urethral and ureteral strictures, should be observed closely during initial days of furosemide treatment. Thereafter, they require observation for worsening of symptoms as excessive diuresis and retention of urine can lead to acute urinary retention leading to acute kidney injury.

Risk of hypokalemia increases with the use of a high dose of furosemide, decreased oral intake of potassium, in patients with hyperaldosteronism states (liver abnormalities or licorice ingestion) or concomitant use of corticosteroid, ACTH, and laxatives.

Furosemide at high doses, i.e., more than 80 mg per day inhibits thyroid hormone binding to thyroid binding protein leading to a transient increase in free thyroid hormones that subsequently causes a mild decrease in total thyroid hormone.[20]

Furosemide was a pregnancy category C drug under the old FDA categories, and clinicians should use caution in pregnant women after discussion with the patient about risk and benefits. Furosemide is known to cross the placenta, and animal reproduction studies have shown adverse events. Although pregnant women with heart failure have had treatment with furosemide, a risk and benefits discussion should take place with the pregnant patient and caution is necessary with the decision to take furosemide during pregnancy; fetal growth will require close monitoring. Additionally, furosemide is secreted in the breastmilk and may lead to suppression of lactation.[21][22][23]

Toxicity

Toxicity with furosemide manifests as extensions of its diuretic activity. Signs and symptoms of overdose or toxicity include dehydration, reduced blood volume, and electrolyte imbalances.[11]

Enhancing Healthcare Team Outcomes

Managing patients with hypervolemia requires an interprofessional team of healthcare depending upon the healthcare setting, outpatient vs. inpatient care. For symptomatic patients with hypervolemia secondary to any of the following conditions; heart failure, liver cirrhosis, or nephrotic syndrome/chronic kidney disease, patients usually need aggressive diuresis. Hospitalized patients requiring aggressive diuretics need care by a multidisciplinary team that includes a nurse, laboratory technologists, pharmacist, and physician.

Careful monitoring of the clinical condition of the patient, daily weight, fluids intake, and urine output, electrolytes, i.e., potassium and magnesium, kidney function monitoring with serum creatinine and serum blood urea nitrogen level is vital to monitor the response to furosemide. Replete electrolytes if indicated as diuresis with furosemide lead to electrolyte depletion, and adjust the dose or even hold off on furosemide if laboratory work shows sign of kidney dysfunction. Similarly, patients who are on furosemide treatment in ambulatory care setting need close monitoring to evaluate for the response to treatment, intermittent electrolytes and kidney function monitoring to replete electrolytes and manage dosing of furosemide as indicated, and to assess for other adverse effects of the furosemide treatment and manage it accordingly.

While the physician (MD, DO, NP, PA) will make the initial decision to treat with furosemide, the entire healthcare team must put forth an interprofessional effort to maintain therapy. Nursing will be on the front lines for monitoring, whether inpatient or outpatient. They can also be the first to assess therapeutic effectiveness and watch for adverse drug reactions. Pharmacists should verify that dosing is appropriate, and to do so, they will need to have received renal and liver function testing results from the team. The pharmacist should also look for drug-drug interactions and alert the physician or nurse if any are present. The pharmacy can also assist the clinician with therapy changes to address the braking phenomenon and ceiling effect. Only with a coordinated interprofessional team effort can furosemide therapy be optimized for positive patient results. [Level V]


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Furosemide - Questions

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Which of the following often requires potassium supplements?



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What is the mechanism of action of furosemide?



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A patient with diabetes mellitus has been taking glipizide 5 mg by mouth daily for the past 4 years. Blood glucose levels have been well controlled. After a recent diagnosis of congestive heart failure, the patient began taking furosemide 40 mg daily by mouth. Which of the following can be expected to develop?



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A 45-year-old male with a history of hypertension, dyslipidemia, coronary artery disease and congestive heart failure presented to the clinic with a complaint of right foot first metatarsophalangeal joint redness, swelling, severe pain for last 2 days. Patient denies fever, chills, trauma, or insect bite. On examination of the right foot, first metatarsophalangeal joint area redness with shiny skin, swelling, and severe tenderness on palpation are observed. No open ulcers or charge is observed. Rest of the exam is benign. Vitals are within normal limits. Home medications are aspirin, clopidogrel, lisinopril, metoprolol, atorvastatin, and furosemide. The joint aspiration reveals many WBCs and negative birefringent needle-shaped crystals without any microorganisms. Which of the following is medication is the most likely cause of the patient's condition?



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A patient with congestive heart failure is prescribed furosemide 20 mg by mouth every morning. What is the reason for this prescription?



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Which of the following diuretics has a high ceiling effect?



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Furosemide is usually supplemented with which of the following solutes?



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A 50-year-old male with a history of congestive heart failure with reduced ejection fraction, coronary artery disease, hypertension, dyslipidemia, CKD stage III presented to the physician's clinic with complaints of decreased hearing in both ears for last 4 weeks. Patient denies any history of ear infection, trauma to the ear or head, ear fullness, nausea, headache or tinnitus. The patient also mentions that 2 months ago the patient was admitted with septic shock secondary to UTI and was treated with broad-spectrum antibiotics including gentamicin and cefepime. Current home medications are aspirin 81 mg/day, metoprolol 50 mg twice a day, atorvastatin 40 mg/day, lisinopril 10 mg/day, furosemide 40 mg twice a day. Patient report no change in heart failure medications since last 6 months. Which of the following is the most likely cause of hearing impairment?



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A 55-year old man presented to the emergency department complaining of difficulty in breathing after little exertion. Upon further questioning, he states the dyspnea is worst on lying down and improves in sitting position. The patient also has a significant past medical history of diabetes mellitus, hypertension, and hyperlipidemia. He further adds that last month he was admitted for the acute myocardial infarction. The physician suspects the diagnosis of CHF and starts furosemide. Which of the following symptoms is most likely to be observed after administering furosemide?



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A 50-year-old female presented to the clinic office for evaluation of bilateral ankle edema present for last 1 month. No other complaints reported by the patient. The patient has a history of hypertension treated with amlodipine and furosemide. Other medications include aspirin, folic acid, and oral contraceptive pills. On examination, bilateral lower extremity edema is evident with no rash or cellulitis. Rest of exam is benign with no signs of cardiac failure or venous stasis. Lab work shows BUN 41 mg/dl, serum creatinine 2 mg/dl. Serum and urine protein electrophoresis are within normal limits. Urinalysis shows high white cell count with eosinophils but no protein, RBC, glucose or bacteria. Renal ultrasound shows increased echogenicity of bilateral renal cortex with no signs of hydronephrosis. Renal biopsy showed acute tubular necrosis, inflammatory cells (lymphocytes and eosinophils) in the tubular epithelium, and interstitium with edema. Which of the following is the most likely cause?



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Which of the following medications acts on the loop of Henle?



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Which of the following is most likely to have orthostatic hypotension as a common complication?



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A 45-year-old male with a history of hypertension, dyslipidemia, coronary artery disease and congestive heart failure presented to the clinic office with a complaint of right foot first toe metatarsophalangeal joint redness, swelling, severe pain for last 2 days. Patient denies fever or chills. Patient denies trauma or insect bite. On examination right foot first, metatarsophalangeal joint area redness with shiny skin, swelling, and severe tenderness on palpation are observed. No open ulcers or charge is observed. Rest of the exam is benign. Vitals are within normal limits. Home medications are aspirin, clopidogrel, lisinopril, metoprolol, atorvastatin, and furosemide. Joint aspiration is performed showing numerous WBCs and negative birefringent needle-shaped crystals. No microorganism is observed. Patient denies a history of gout in the past and no family history of gout. What is the most likely mechanism of action of new-onset gouty arthritis?



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Where is the site of action of furosemide?



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Which of the following diuretics can cause ototoxicity?



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A 24 month old with congenital heart disease is on furosemide and digoxin. Which electrolyte imbalance is most likely?



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Furosemide works at which of the following?



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How long does it take IV furosemide to cause diuresis?



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Which is not a common adverse effect of furosemide?



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Which drug classification is furosemide?



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What is the mechanism of furosemide?



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Which of the following parameters should be monitored when administering furosemide?



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An 82-year-old female with a history of heart failure with reduced ejection fraction is admitted for evaluation of lightheadedness. The patient reports that she is feeling lightheaded and generalized weak for last 1 week. Lightheadedness is more pronounced when the patient stands up from sitting position. The patient feels thirsty and reports having a weight loss of 4 pounds over the last 1 week. No nausea, vomiting, spinning sensation of head, changes in hearing, tinnitus or ear discharge is reported. The patient denied syncope, palpitation, chest pain, and shortness of breath. Vitals are: Blood pressure 110/80 mmHg, pulse 100 bpm, respiratory rate 20/min, pulse ox 93% on room air, temperature 97 °F. Orthostatic vitals are positive. The patient appears dry with no leg edema and oral mucosa is dry. The chest is clear to auscultation. S1 plus S2 plus no additional sound. No bilateral lower extremity edema. No focal motor or sensory deficit. Patient is taking aspirin, carvedilol, atorvastatin, lisinopril, furosemide. EKG shows normal sinus rhythm and no acute ischemia. Echocardiogram performed showed ejection fraction of 37% with no new changes compared to the prior study performed within last 6 months. Basic metabolic profiles shows acute kidney injury with serum creatinine of 1.7 mg/dL and basic urea nitrogen of 40. Baseline serum creatinine is 1.1 mg/dL. Serum potassium was 2.9 milliequivalents per liter. What is the most common drug contributing to the current clinical condition?



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Lasix is the brand name for which generic drug?



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Furosemide is correctly classified as which of the following?



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A nurse is educating a patient regarding furosemide use and its potential complications. Which of the following would be appropriate teaching points to incorporate in the teaching session? Select all that apply.



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A nurse is caring for a client with congestive heart failure who is on IV furosemide 40 mg daily. What are essential aspects of nursing care and education for this client? Select all that apply.



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A 68-year old client is admitted to the intensive care unit with congestive heart failure. She is placed on BiPap until diuresis is effective in relieving the pulmonary congestion. It is decided to perform diuresis with furosemide. Which of the following are adverse effects of this medication? Select all that apply.



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A patient in heart failure is started on long-term furosemide. Which of the following adverse effects are most likely in long-term therapy? Select all that apply.



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Furosemide - References

References

American Geriatrics Society 2015 Updated Beers Criteria for Potentially Inappropriate Medication Use in Older Adults. Journal of the American Geriatrics Society. 2015 Nov;     [PubMed]
Brater DC,Chennavasin P,Day B,Burdette A,Anderson S, Bumetanide and furosemide. Clinical pharmacology and therapeutics. 1983 Aug;     [PubMed]
Felker GM,Lee KL,Bull DA,Redfield MM,Stevenson LW,Goldsmith SR,LeWinter MM,Deswal A,Rouleau JL,Ofili EO,Anstrom KJ,Hernandez AF,McNulty SE,Velazquez EJ,Kfoury AG,Chen HH,Givertz MM,Semigran MJ,Bart BA,Mascette AM,Braunwald E,O'Connor CM, Diuretic strategies in patients with acute decompensated heart failure. The New England journal of medicine. 2011 Mar 3;     [PubMed]
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K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. American journal of kidney diseases : the official journal of the National Kidney Foundation. 2004 May     [PubMed]
Runyon BA, Introduction to the revised American Association for the Study of Liver Diseases Practice Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology (Baltimore, Md.). 2013 Apr     [PubMed]
Shankar SS,Brater DC, Loop diuretics: from the Na-K-2Cl transporter to clinical use. American journal of physiology. Renal physiology. 2003 Jan     [PubMed]
Ponto LL,Schoenwald RD, Furosemide (frusemide). A pharmacokinetic/pharmacodynamic review (Part I). Clinical pharmacokinetics. 1990 May     [PubMed]
Hammarlund MM,Paalzow LK,Odlind B, Pharmacokinetics of furosemide in man after intravenous and oral administration. Application of moment analysis. European journal of clinical pharmacology. 1984     [PubMed]
Haegeli L,Brunner-La Rocca HP,Wenk M,Pfisterer M,Drewe J,Krähenbühl S, Sublingual administration of furosemide: new application of an old drug. British journal of clinical pharmacology. 2007 Dec     [PubMed]
Brater DC, Diuretic therapy. The New England journal of medicine. 1998 Aug 6     [PubMed]
Vargo DL,Kramer WG,Black PK,Smith WB,Serpas T,Brater DC, Bioavailability, pharmacokinetics, and pharmacodynamics of torsemide and furosemide in patients with congestive heart failure. Clinical pharmacology and therapeutics. 1995 Jun     [PubMed]
Vasko MR,Cartwright DB,Knochel JP,Nixon JV,Brater DC, Furosemide absorption altered in decompensated congestive heart failure. Annals of internal medicine. 1985 Mar     [PubMed]
Sheffield PA,Turner JS Jr, Ototoxic drugs: a review of clinical aspects, histopathologic changes and mechanisms of action. Southern medical journal. 1971 Mar     [PubMed]
Wigand ME,Heidland A, Ototoxic side-effects of high doses of frusemide in patients with uraemia. Postgraduate medical journal. 1971 Apr     [PubMed]
Bornstein SR,Allolio B,Arlt W,Barthel A,Don-Wauchope A,Hammer GD,Husebye ES,Merke DP,Murad MH,Stratakis CA,Torpy DJ, Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. The Journal of clinical endocrinology and metabolism. 2016 Feb     [PubMed]
Newnham HH,Hamblin PS,Long F,Lim CF,Topliss DJ,Stockigt JR, Effect of oral frusemide on diagnostic indices of thyroid function. Clinical endocrinology. 1987 Apr     [PubMed]
Riva E,Farina P,Tognoni G,Bottino S,Orrico C,Pardi G, Pharmacokinetics of furosemide in gestosis of pregnancy. European journal of clinical pharmacology. 1978 Dec 18     [PubMed]
Johnson-Coyle L,Jensen L,Sobey A, Peripartum cardiomyopathy: review and practice guidelines. American journal of critical care : an official publication, American Association of Critical-Care Nurses. 2012 Mar     [PubMed]
Garg J,Palaniswamy C,Lanier GM, Peripartum cardiomyopathy: definition, incidence, etiopathogenesis, diagnosis, and management. Cardiology in review. 2015 Mar-Apr     [PubMed]
Ellison DH,Felker GM, Diuretic Treatment in Heart Failure. The New England journal of medicine. 2017 Nov 16;     [PubMed]
Wilcox CS,Mitch WE,Kelly RA,Skorecki K,Meyer TW,Friedman PA,Souney PF, Response of the kidney to furosemide. I. Effects of salt intake and renal compensation. The Journal of laboratory and clinical medicine. 1983 Sep;     [PubMed]

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