Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bumetanide2 is a new diuretic with a rapid onset and short duration of action. It is advocated for the treatment of oedema of cardiac origin; that associated with cirrhosis of the liver and renal diseases, including the nephrotic syndrome oedema of pregnancy and in pulmonary oedema. Bumetanide produces a pattern of water and electrolyte excretion closely resembling that of frusemide although it differs structurally from frusemide and other diuretics. 1 mg of bumetanide produces a diuretic effect similar to that evoked by 40 to 60 mg of frusemide. Short-and long-term studies in oedema of varying aetiology have shown bumetanide to be an effective diuretic. Because it is chemically different from existing diuretics, bumetanide may be helpful in oedema resistant to other drugs. It is well tolerated, but like other natriuretics it causes hypericaemia and may cause hypokalaemia during long-term administration.
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PMID:Bumetanide: A preliminary report of its pharmacological properties and therapeutic efficacy in oedema. 112 4

The effect of decreases in plasma colloid osmotic pressure (COP) on the development of lung edema was studied in nephrotic rats. Five control animals were compared with five animals with nephrotic syndrome induced by administration of anti-rat glomerular basement membrane antibody. The COP and the left ventricular diastolic pressure (LVDP) were significantly decreased in nephrotic rats. However, no significant differences were seen in the COP - LVDP gradient, weight-to-dry lung weight ratio, or arterial oxygenation between the nephrotic and control animals. These data suggest that decreases in COP during nephrosis are not associated with accumulation of extravascular lung water.
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PMID:Absence of lung edema in nephrotic rats. 376 Jun 75

Bumetanide is a potent 'loop' diuretic for the treatment of oedema associated with congestive heart failure, hepatic and renal diseases, acute pulmonary congestion and premenstrual syndrome and in forced diuresis during and after surgery. Bumetanide may be given orally, intravenously or intramuscularly and produces a rapid and marked diuresis, and increased urinary excretion of sodium, chloride and other electrolytes (within 30 minutes) which persists for 3 to 6 hours. Its principal site of action is on the ascending limb of the loop of Henle, with a secondary action on the proximal tubule. Pharmacologically, bumetanide is about 40-fold more potent than frusemide (furosemide), with the exception of its effects on urinary potassium excretion where its potency is lower. Studies in patients with oedema due to congestive heart failure, pulmonary oedema or hepatic disease show that oral or intravenous bumetanide 0.5 to 2 mg/day produces results comparable to those with frusemide 20 to 80 mg/day. In acute pulmonary oedema, intravenous bumetanide produces a very rapid diuresis. Higher doses of bumetanide may be required (up to 15 mg/day) in patients with chronic renal failure or nephrotic syndrome. In these patients muscle cramps are not uncommon with bumetanide, but glomerular filtration rates are unaffected. In most studies, diuretic effects were accompanied by decreased bodyweight, abdominal girth and improvements in a variety of haemodynamic parameters. Comparison of bumetanide with frusemide at a dose ratio of 1 : 40 reveals no significant differences in clinical response with the exception of renal disease, where patients with oedema appear to respond better to bumetanide. Combination with thiazide diuretics enhances the clinical response to bumetanide. Potassium supplements and spironolactone may be beneficial additions to bumetanide where patients at risk of hypokalaemia can be identified. Clinically important side effects are infrequent, with audiological impairment occurring to a lesser extent than with frusemide. Bumetanide thus offers an important alternative to frusemide when a 'loop' diuretic is indicated.
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PMID:Bumetanide. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic use. 639 89

A 14-year-old girl with sickle cell disease and nephrotic syndrome developed bone pain, followed by pulmonary edema, seizures, coma, and bilateral flaccid paralysis. Fat embolism syndrome was diagnosed by cranial magnetic resonance imaging and an exchange transfusion was performed. Within 3 months, all symptoms had resolved. It is concluded that fat embolism syndrome must be considered as a possible cause of acute neurologic deterioration in patients with sickle cell anemia.
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PMID:Nontraumatic fat embolism syndrome in sickle cell anemia. 774 67

A 32 year old man was admitted for dyspnea, hemoptysis, macroscopic hematuria, hypertension (140/100), peripheral edema and hemodynamic decompensation. Lung Xrays revealed pulmonary edema and a cavity in the left apex. Laboratory determinations revealed an altered renal function with increased creatinine and urea levels and nephrotic syndrome. There was leucocyturia, hematuria and cylindruria. The sputum showed a large number of acid-fast bacilli. The patient began anti-tuberculosis treatment with three drugs (isoniacid, rifampicin, pirazinamide). On ultrasonography, both kidneys revealed ecogenic lesions with size, shape and cortico-medular relationship preserved. The patient persisted with altered renal function, steady levels of urea nitrogen, creatinine and potassium, preserved diuresis and hypertension. Bidimensional echocardiogram: LVDD 55 mm, hypoquinetic septum, pericardic effusion, thickened pericardium, pleural effusion, shortening fraction decreased. He received treatment for this congestive cardiac failure and hypertension with enalapril, nifedipine and fursemide. A percutaneous renal biopsy was performed with anatomopathologic diagnosis of diffuse encocapillar proliferative glomerulonephritis with crescents (15%) and total glomerular sclerosis (33%). Immunofluorescence: positive, immune-complexes with IgM and C3. The patient gradually recovered his normal renal function, improved his pleural effusions and normalized his cardiac function. He was discharged in good clinical condition on the 69th day of anti-tuberculosis treatment. An association between pulmonary tuberculosis and glomerulonephritis is discussed. It is proposed that renal lesions might be the consequence of the tuberculosis due to the sedimentation of circulating immune-complexes.
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PMID:[Immune complex glomerulonephritis associated with pulmonary tuberculosis]. 785 90

We report a case of hypocomplementemic urticarial vasculitis syndrome (HUVS) with membranous glomerulopathy in a 62-year-old man who had a 2-month history of secondary iritis. He was transferred to our hospital because of uncontrollable edema and respiratory dysfunction. Physical examination revealed anasarca, pulmonary edema, hypertension and urticaria-like eruption on his arms. Urinalysis, blood chemistry and serological studies showed massive proteinuria (10.5g/day) with numerous granular casts, hypoalbuminemia (1.5g/dl), renal dysfunction (creatinine; 1.6mg/dl, BUN; 86mg/dl), hypercholesterolemia (total cholesterol; 455mg/dl), positive results for antinuclear factor, microsome test, thyroid test, lupus anticoaglant, antithyroglobulin test and rheumatoid factor, but LE cell or double-strand anti DNA antibody was negative. Serum complement levels were persistently low as CH50 of 13 U/ml and Clq of 6.0 micrograms/dl. The patient serum precipitated with normal human Clq by immunodiffusion analysis, indicating the presence of anti-Clq antibody. Renal biopsy revealed membranous glomerulopathy with prominent fine granular deposition of Clq along the glomerular basement membrane by immunofluorescent study and subepithelial dense deposit by electron microscopy. Corticosteroid treatment was ineffective for hypocomplementemia and nephrotic syndrome. Acute subendocardial infarction occurred on the 25th hospital day and he died of acute respiratory distress syndrome on the 45th hospital day. Autopsy revealed leucocytoclastic vasculitis in the alveolar wall. HUVS was confirmed by clinical symptoms, such as iritis and urticaria-like eruption, serum anti-Clq antibody, the absence of any specific autoantibody for systemic lupus erythematosus (SLE) and leucocytoclastic vasculitis in the alveolar wall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nephrotic syndrome due to membranous glomerulopathy in hypocomplementemic urticarial vasculitis syndrome;--a case report]. 807 26

Numerous agents have been associated with minimal change disease. We describe a previously unreported association in a 45-year-old white woman of scuba diving exposure to fire coral (Millepora species) that was followed by the development of nephrotic syndrome, acute renal failure, pulmonary edema, and intubation. The renal biopsy specimen was consistent with minimal change disease. Institution of corticosteroid therapy resulted in symptomatic improvement and resolution of proteinuria. Physicians, particularly those in scuba-diving areas, should consider minimal change disease in exposed patients with proteinuria because a prompt diagnostic and therapeutic approach may potentially limit complications.
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PMID:Minimal change disease in association with fire coral (Millepora species) exposure. 1637 75

Hypertension and episodic pulmonary oedema are known complications of bilateral renovascular disease. However, significant proteinuria has not been reported in this setting. We describe a patient who presented with recurrent pulmonary oedema and nephrotic syndrome, and was found to have bilateral renal artery stenosis. Percutaneous angioplasty and stenting led to a complete resolution of both, confirming a causal relationship. This is perhaps the first report documenting the rare combination of nephrotic syndrome and flash pulmonary oedema due to bilateral renal artery stenosis.
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PMID:Nephrotic syndrome and recurrent pulmonary oedema in bilateral atherosclerotic renal artery stenosis: resolution following renal angioplasty and stenting. 1720 79

Hypoalbuminemia is common in patients with heart failure, and this condition becomes more prevalent with increasing age and illness. Hypoalbuminemia is thought to result mainly from malnutrition, inflammation and cachexia. Other causal factors include hemodilution, liver dysfunction, protein-losing enteropathy, increased transcapillary escape rate, and nephrotic syndrome. According to Starling's law, low plasma oncotic pressure related to hypoalbuminemia induces a fluid shift from the intravascular to the interstitial space, and there is now clinical evidence that hypoalbuminemia facilitates the onset of cardiogenic pulmonary edema. Hypoalbuminemia has emerged as an independent predictor of incident heart failure in end-stage renal disease and elderly patients. Recent data also suggest that hypoalbuminemia provides prognostic information incremental to the usual clinical and biochemical variables in patients with heart failure regardless of clinical presentation. The presence of hypoalbuminemia in patients with heart failure may have potential therapeutic consequence in clinical practice. If present, subclinical excess of fluid must be removed. A dietary survey should also be performed, and renutrition may be indicated. It is unknown whether targeted nutritional intervention and albumin administration confer benefits to hypoalbuminemic patients with heart failure, and further research is warranted in this setting.
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PMID:Human serum albumin in the clinical syndrome of heart failure. 2162 32

Primary bacterial peritonitis is a rare complication of idiopathic nephrotic syndrome (INS) in children, found in 1.5-3.7% cases. The 10-year-old girl was admitted with INS relapse: generalized edema, proteinuria 630 mg/kg/24 h, hypoalbuminemia 1.8 g/dL, hypogammaglobulinemia 74.0 mg/dL (n: 618-1537 mg/dL), GFR 71.6 mL/min/1.73 m2. She was treated with prednisone 60 mg/24 h. On 5th day severe pain, fever, CRP (15.5 mg/dL) and leukocytosis (19.5 tys/mm3) rise occurred. On 6th day due to suspicion of peritonitis, laparotomy was performed and 400 mL of suppurative exudate was evacuated (Streptococcus pneumoniae was cultured). Postoperative course was complicated with acute kidney injury (GFR 47.7 mL/min/ 1.73 m2), lung edema, arterial hypertension, and separation of the layers of a surgical wound. The patient was treated with: imipenem (9 days), vancomycine i.v. (4 days)/p.o. (11 days) (Clostridium difficile toxin present in stool), fluconazole (14 days), 20% albumins, furosemide, labetalole, cyclosporine A (started on 56th day after the operation due to secondary steroid-resistance of INS). The remission was achieved after 7 days of cyclosporine A treatment. Authors suggest that children with nephrotic syndrome belong to high-risk group of invasive pneumococcal disease, therefore they require careful implementation of mandatory immunization schedule. Peritonitis is a rare and still dangerous infectious complication of nephrotic syndrome in children.
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PMID:[Steroid-resistant nephrotic syndrome complicated with severe Streptococcus pneumonlae peritonitis in a 10-year-old girl--case report]. 2449 Apr 66


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