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)

A 66-year-old female with bilateral ureteral tumors associated with chronic renal failure is presented. She received pan-hysterectomy due to uterine cancer in 1957. She was first referred to our clinic to make internal shunt under a diagnosis of chronic renal failure. In 1979, the diagnosis of neurogenic bladder and bilateral vesicoureteral reflux (rt; grade 3, lt; grade 1) was made. She was admitted to our clinic with complaints of macroscopic hematuria and a temperature of 39 degrees C on April 28, 1983. Cystoscopically, pyuria from the right ureteral orifice was found. Right retrograde pyelography revealed severe dilatation of the right ureter and renal pelvis with some filling defects. For drainage of pus retaining in the right renal pelvis, right percutaneous nephrostomy was made under the guidance of ultrasonography. After her general condition improved, right nephroureterectomy was performed under the diagnosis of right pyonephrosis on June 8, 1983. Right pyelonephritis and right ureteral tumor, grade 3, were pathologically demonstrated. After the operation, an invasive bladder tumor was detected on cystoscopy and ultrasonography, subsequently a total of 3,900 rad irradiation was given to the bladder tumor. She died of pulmonary edema 7 months later. Autopsy demonstrated a transitional carcinoma, grade 3, of the left ureter. Bilateral urothelial tumors of the upper urinary tract is rare, and to our knowledge only 29 cases have been reported in Japan.
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PMID:[Bilateral ureteral tumors associated with chronic renal failure: a case report]. 332 59

Achromobacter xylosoxidans is an uncommon nosocomial pathogen known to cause many serious infections. A 69-year-old woman with diabetes mellitus and chronic renal failure was admitted with pulmonary edema. The patient developed fever and pulmonary infiltrate with bilateral pleural effusions while she was on a respirator in the intensive care unit. Culture of sputum, pleural fluid and blood grew A. xylosoxidans. Bilateral chest tubes were inserted and the patient was treated for one month with piperacillin and trimethoprim-sulfamethoxazole. Gradual response, both clinically and radiologically, was noted after prolonged therapy. A review of the literature on infections due to A. xylosoxidans, the unique susceptibility pattern of the organism to various antibiotics and the use of combination therapy in Achromobacter infections are discussed.
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PMID:Infections due to Achromobacter xylosoxidans. Case report and review of the literature. 381 5

Results of using the method of sequential ultrafiltration with hemodialysis and that of hemodiafiltration in the treatment of 70 patients with acute and chronic renal failure in terminal states are described. The patients were under observation in the course of 202 procedures of hemodiafiltration and 175 sequential ultrafiltration with hemodialysis. Apart from this, 21 procedures of isolated ultrafiltration were carried out in patients with pronounced cardiac failure, irreversible pulmonary edema resulting from acute myocardial infarction and heart diseases. Sequential ultrafiltration and hemodialysis were performed by means of home-produced equipment SGD using Cuprofan dialysis film and capillary dialyzators. The volume of ultrafiltration ranged from 1 to 8 litres/procedure at a rate of 17-500 ml/min, at a transmembrane pressure 100-400 mmHg. It was found that sequential ultrafiltration with hemodialysis was indicated for patients in terminal states complicated by renal failure in the presence of severe fluid retention, pulmonary edema, patients with low tolerance to hemodiafiltration, and those in critical states (including irreversible pulmonary edema) of cardiological genesis.
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PMID:Resuscitation aspects of ultrafiltration and haemodialysis. 630 96

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

Little is known of the effect of chronic renal failure (CRF) on ventilatory regulation. In 38 subjects (19 healthy, 19 with CRF before and after dialysis), we performed measurements of ventilation (VE) and occlusion pressure (P0.1) while the subjects were breathing air and hypercapnic gas mixtures. The results have shown that (1) during air ventilation, CRF patients exhibited lower values of VE and P0.1, which returned to normal after dialysis; (2) during hypercapnic ventilation, CRF patients had the same response as healthy subjects for VE but higher P0.1; hemodialysis induced an upward shift of the CO2 response curve in CRF patients. A twofold mechanism is probably involved: pulmonary edema, which reduces lung elasticity, and neuromuscular hypoexcitability, both implying a stronger central command.
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PMID:Ventilatory and occlusion pressure responses to hypercapnia in patients with chronic renal failure. 643 71

Metastatic pulmonary calcification (MPC), a complication of chronic renal failure, is uncommonly diagnosed antemortem, yet may be a significant etiology of pulmonary dysfunction in patients with renal failure. The degree of respiratory distress often does not correlate with the degree of macroscopic calcification. Patients with extensive calcification may be asymptomatic, while others with subtle calcification or normal chest radiographs may have severe respiratory compromise. Additionally, the findings on chest radiographs may be confused with air-space disease, including pulmonary edema and pneumonia. Radionuclide imaging may detect MPC in the setting of normal chest radiographs, and confirm the diagnosis when there are radiographic findings of air-space disease without macroscopic calcification. We present a patient with bilateral upper lobe disease suspected to represent edema or pneumonia, proven to represent MPC on 99mTc MDP scintigraphy with single photon emission computed tomography (SPECT), CT, and later at transbronchial biopsy.
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PMID:Metastatic pulmonary calcification mimicking air-space disease. Technetium-99m-MDP SPECT imaging. 777 54

Two patients with asymptomatic IgA nephropathy (IgAN) and a third patient with chronic renal failure due to IgAN died following a recent onset of dyspnea, hemoptysis, and pulmonary infiltrates. In all cases, the cause of death was respiratory failure attributed to either bronchopneumonia or pulmonary edema. However, no infectious agent was identified. In all three patients, the diagnoses of IgAN and idiopathic pulmonary hemorrhage were established at postmortem examination. Acute alveolar hemorrhage was present in two patients. All three patients had heavy alveolar hemosiderin-laden macrophages, and capillaritis was recognized in two of them. The occurrence of fatal pulmonary hemorrhage in patients with IgAN is rare. Our findings suggested an immune complex-mediated pulmonary injury that was possibly related to the systemic nature of IgAN.
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PMID:Pulmonary hemorrhage. A fatal manifestation in IgA nephropathy. 819 62

Despite broader indications and easier access to renal replacement therapy during the past decades in Western countries, an unduly high number of patients is still referred to maintenance hemodialysis (HD) at a very advanced stage of chronic renal failure (CRF). To assess whether such late referral induces detrimental effects, we retrospectively compared clinical status and laboratory features in 20 patients who had been referred to us less than one month prior to first HD (late referral, or LR group) and in 20 sex- and age-matched controls who had undergone regular follow-up for at least six months prior to HD (early referral, or ER group). Male to female ratio was 12/8 and age averaged 53.5 years in both groups. Mean (+/- 1 SD) systolic and diastolic blood pressure were higher in LR group than in controls (180 +/- 14/102 +/- 10 vs. 153 +/- 15/86 +/- 7 mm Hg, P < 0.001) and fluid overload with pulmonary edema was present in 13/20 versus 3/20 patients (P < 0.001). Plasma concentrations (mmol/liter) of creatinine (1.12 +/- 0.27 vs 0.97 +/- 0.11, P < 0.01) and phosphate (2.58 +/- 0.47 vs. 1.92 +/- 0.31, P < 0.001) were higher, whereas plasma levels of bicarbonate (14.2 +/- 3.9 vs 22.5 +/- 4.2, P < 0.001) and calcium (1.85 +/- 0.24 vs. 2.27 +/- 0.15, P < 0.001) were lower in LR than in ER group, as were hemoglobin (7.1 +/- 1.1 vs. 9.4 +/- 0.9 g/dl, P < 0.001) and serum albumin levels (35.3 +/- 4.8 vs. 39.7 +/- 3.4, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detrimental effects of late referral in patients with chronic renal failure: a case-control study. 832 Sep 13

It has been postulated that patients with chronic renal failure, even in the absence of cardiopulmonary symptoms, accumulate interstitial pulmonary fluid, which is removed by haemodialysis. To test this hypothesis we used the indocyanine green (ICG)-heavy water double indicator dilution method to measure lung water, cardiac output, and central blood volume in relation to haemodialysis. Ten uraemic patients, without cardiopulmonary symptoms, were investigated at the beginning and end, and 2 h after, a regular dialysis session. A group of 18 surgical patients about to undergo elective abdominal surgery served as controls. Despite normal gas exchange, central blood volume, and cardiac output at the start of dialysis the mean (SD) lung water was significantly higher than in the control group [4.8 (0.9) compared with 3.6 (0.7) ml/kg, P < 0.001]. There was no correlation between weight gain between sessions of dialysis and the magnitude of lung water at the start of dialysis. Lung water decreased (P < 0.001) to the level of the control group in response to dialysis. There was no correlation between weight loss and reduction in lung water induced by dialysis. In conclusion, we have verified the presence of subclinical pulmonary oedema which was removed by dialysis in a group of patients with established renal failure. The variations in lung water cannot be explained by hydrostatic mechanisms alone.
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PMID:Subclinical pulmonary oedema and intermittent haemodialysis. 894 89

The sudden onset of pulmonary edema in patients with renal artery stenosis is an increasingly recognized entity. Some data also support an association between renal artery stenosis and chronic cardiac failure. We report a 60-year-old man with chronic renal failure who had most normal arterial blood pressure despite highly severe chronic congestive heart failure. Renovascular disease was suspected and an arteriography revealed very tight bilateral artery stenosis. Removal of stenosis led to both renal and cardiac functions improvement.
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PMID:Chronic congestive heart failure associated with bilateral renal artery stenosis. 924 81


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