Furosemide renal disease

Loop diuretics are used in the treatment of edema associated with CHF, cirrhosis of the liver, and renal disease, including the nephrotic syndrome. These drug s are particularly useful when a greater diuretic effect is desired. Furosemide is the drug of choice when a rapid diuresis is needed or if the patient has renal insufficiency. Furosemide and torsemide are also used to treat hypertension. Ethacrynic acid is also used for the short-term management of ascites caused by a malignancy, idiopathic edema, or lymphedema. 

Edema Edema associated with CHF, hepatic cirrhosis, and renal disease, including the nephrotic syndrome. Particularly useful when greater diuretic potential is desired. Parenteral administration is indicated when a rapid onset of diuresis is desired (eg, acute pulmonary edema), when Gl absorption is impaired or when oral use is not practical for any reason. As soon as it is practical, replace with oral therapy. Hypertension (furosemide, oral torsemide, oral) A one or in combination with other antihypertensive drugs. 

Furosemide is eliminated in equal portions by renal and non-renal (glucuronidation) routes. Its half-life is prolonged in renal failure, but hepatic failure has little effect, Bumetanide and torasemide are eliminated via CYP isoenzymes and so their half-life is affected by hepatic disease more than renal disease. They are known to cause thrombocytopenia (hut decrease activity of oral anticoagulants), ototoxicity and nephrotoxicity. 

Renal disease (uraemia) may increase the volume of distribution of acidic drugs that extensively bind to plasma albumin (e.g., phenytoin, valproic acid, naproxen, phenylbutazone, furosemide). As decreased protein binding would increase the unbound (free) fraction in the plasma, the therapeutic concentration range (based on total drug concentration) would be lower than the usual... 

Approximately 65% of furosemide is excreted unchanged in the urine, and the remainder is conjugated to glucuronic acid in the kidney. Accordingly, in patients with renal, but not fiver, disease, the elimination half-life of furosemide is prolonged. In contrast, bumetanide and torsemide have significant hepatic metabolism, so the elimination half-lives of these loop diuretics are prolonged by liver, but not renal, disease. 

Furosemide possesses relatively high effieaey, rapid onset of action, short duration of action, and 1 10 ratio between the minimum and maximum diuretie dose. It is used for the treatment of oedema associated with renal disease, nephrotic syndrome, cirrhosis of the liver and congestive heart failure. It has an edge over other commonly used diuretic agents specifically when a greater diuretic potential is required. It may also be employed towards the management of hypertension. 

Similar to furosemide. Narrower dose-response curve than furosemide. Increased azotemia in patients with renal disease taking tetracycline. Ethacrynate sodium is used intravenously to treat acute pulmonary edema. 

Loop diuretics are used cautiously in patients with renal dysfunction. The loop diuretics are Pregnancy Category B (ethacrynic acid and torsemide) and C drugp (furosemide and bumetanide) and must be used cautiously during pregnancy and lactation. Furosemide is used in children but should be used cautiously. The loop diuretics are used cautiously in patients with liver disease, diabetes, lupus erythematosus (may exacerbate or activate the disease), or diarrhea. Patients with... 

A 62-year-old woman developed acute renal insufficiency after using topical ketoprofen for 5 days (11). She had several predisposing factors to NSAID-induced acute renal insufficiency, such as advanced age, chronic renal impairment due to polycystic kidney disease, and treatment with an ACE inhibitor and furosemide. 

A 70-year-old man developed heart failure secondary to ischemic heart disease and severe aortic stenosis (1). Furosemide 20 mg/day was replaced by torasemide 5 mg/day. After the second dose he developed oliguria and an erythematous morbilliform rash with palpable violet petechial lesions on the legs. Chest X-ray showed bilateral alveolar infiltrates. Serum creatinine and potassium were raised (212 pmol/1 and 6.7 mmol/1 respectively). Skin biopsy showed leukocytoclastic vasculitis. After withdrawal of torasemide, his renal function improved (serum creatinine 97 pmol/1) and the skin lesions resolved (leaving residual pigmented areas) within 8 days. 

The risk of ACE inhibitor-induced renal impairment in patients with or without renovascular disease can be potentiated by diuretics. " In an analysis of 74 patients who had been treated with captopril or lisinopril, reversible acute renal failure was more coimnon in those who were also treated with a diuretic (furosemide and/or hydrochlorothiazide) than those who were not (11 of 33 patients compared with 1 of 41 patients). Similarly, in a prescription-event monitoring study, enalapril was associated with raised creatinine or urea in 75 patients and it was thought to have contributed to the deterioration in renal function and subsequent deaths in 10 of these patients. However, 9 of these 10 were also receiving loop or thiazide diuretics, sometimes in high doses. Retrospective analysis of a controlled study in patients with hypertensive nephrosclerosis identified 8 of 34 patients who developed reversible renal impairment when treated with enalapril and various other antihypertensives including a diuretic (furosemide or hydrochlorothiazide). In contrast, 23 patients treated with placebo and various other antihypertensives did not develop renal impairment. Subsequently, enalapril was tolerated by 7 of the 8 patients without deterioration in renal function and 6 of these patients later received diuretics. One patient was again treated with enalapril with recurrence of renal impairment, but discontinuation of the diuretics (furosemide, hydrochlorothiazide, and triamterene) led to an improvement in renal function despite the continuation of enalapril. ... 

The clinical documentation seems to be limited to these reports. It appears to be a combination of a drug-drug interaction (clofibrate with furosemide) with or without a drug-disease interaction (clofibrate with nephrotic syndrome). The authors of one report suggest that serum proteins and renal function should be checked before giving clofibrate to any patient. If serum albumin is low, the total daily dosage of clofibrate should not exceed 500 mg for each 1 g per 100 mL of the albumin concentration. However, note that this guidance is old. 

Severe multisystem trauma, endotoxemia, or situations in which there is a raised metabolic demand for thiamin, such as pregnancy, thyrotoxicosis, and intercurrent illness or impaired absorption (e.g., alcohol abuse or gastrointestinal disease or resection), can produce subclinical evidence of thiamin deficiency or more severe life-threatening aspects of beriberi, such as renal and/or cardiovascular failure. The elderly may be particularly at risk of subclinical thiamin deficiency. One Belgian study on patients with a mean age of 83 years reported that 40% had a raised TDP effect (>15%), in whom there was a high proportion of Alzheimer s disease, depression, cardiac failure, and falls. The diuretic furosemide was also more frequently taken by the thiamin-deficient patients. 

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