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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 7 years (1981-1988) at the Kenyatta National Hospital (KNH), Nairobi the diagnosis of systemic lupus erythematosus (SLE) was made in 67 patients. In 23 of these patients lupus nephritis complicated the SLE. Lupus nephritis was diagnosed through renal biopsy, haematuria and proteinuria in urine with positive lupus erythematosus (LE) cell phenomenon. The histology found in these patients included 5 patients with minimal lesion, 7 patients with membranous, 3 with focal, 4 with diffuse, 3 with crescenteric and one with membranoproliferative glomerulonephritis. While patients with minimal, membranous and focal nephritis had general good outlook on low dose maintenance or intermittent high dose steroid therapy the others with diffuse, crescenteric and membranoproliferative nephritis had poor prognosis. Patients with diffuse proliferative, membranoproliferative and crescenteric nephritis tended to have septicaemia, pulmonary oedema, fluid overload and chronic renal failure with poor prognosis. These patients responded poorly to oral and parenteral steroid therapy whether high or low dose.
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PMID:Management of lupus nephritis at the Kenyatta National Hospital. 227 66

A 61 year old man presented with mitral regurgitation and glomerulonephritis caused by suspected infective endocarditis. His glomerulonephritis remitted on immunosuppression but mitral valve replacement with a Carpentier-Edwards porcine xenograft later proved necessary. The patient became dialysis dependent and cadaveric renal allografting was complicated by delayed graft function and refractory pulmonary oedema. Cardiac catheterisation showed severe calcification and stenosis of the xenograft with a transvalvar gradient of 23 mm Hg and despite emergency valve replacement the patient died. The valve had been in place less than five years. The rapid calcification and stenosis of a bioprosthetic heart valve calls into question the use of such prostheses in patients with chronic renal failure.
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PMID:Calcific stenosis of a mitral valve xenograft in a patient in chronic renal failure. 266 2

Alveolar hemorrhage (AH) is the result of diffuse bleeding into the acinar portion of the lung. Cardinal symptoms of AH include hemoptysis, dyspnea, alveolar filling opacities on chest roentgenogram, anemia and hypoxemia. However, AH is often misdiagnosed as pneumonia or pulmonary edema at the time of initial presentation. Isolated AH may occur but is more often seen in diffuse connective tissue diseases or in rapidly progressive glomerulonephritis. - At the Medical Clinic of the University Hospital of Zurich we have diagnosed AH in 18 patients (13 males, 5 females) over the last ten years (1978-1988). In 2 patients AH occurred as an isolated symptom: once due to occupational inhalation of fumes containing trimellitic anhydride, and once as so-called idiopathic pulmonary hemosiderosis. In 16 patients AH was associated with kidney disease, including the following disorders: vasculitis and collagen vascular disorders (9), rapidly progressive glomerulonephritis (4) and Goodpasture's syndrome (3). In 5 patients the presenting symptom was AH. 9 patients presented initially with renal symptoms and in 2 patients renal and pulmonary features occurred simultaneously. 7 patients died of the underlying disease or its complications. Both patients with isolated AH have survived. In the remaining 9 patients 1 required dialysis temporarily and 4 permanently. All patients except the one with AH due to inhalation of trimellitic anhydride were treated with immunosuppressive agents. - Since the pulmonary features are similar in each of the AH syndromes, diagnosis of the underlying disorder is heavily dependent upon pathologic evaluation of diseased extrapulmonary organs. Moreover, immunologic studies are essential. Failure to diagnose or treat AH syndromes in the early stages may have lethal consequences.
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PMID:[Alveolar hemorrhage]. 268 52

Diffuse pulmonary hemorrhage is an uncommon condition that is difficult to differentiate radiographically from diffuse pneumonia or pulmonary edema. The diagnosis should be suspected when a patient has even mild hemoptysis or has one of the diseases known to be associated with diffuse pulmonary hemorrhage. This paper reviews the clinical and radiographic features of diffuse pulmonary hemorrhage and presents a classification scheme depicted as a Venn diagram formed by four overlapping circles representing pulmonary hemorrhage, renal disease, immune complex disease, and antiglomerular basement membrane (anti-GBM) disease. This scheme results in six categories of pulmonary hemorrhage: associated with glomerulonephritis and anti-GBM antibody; associated with renal disease without demonstrable immunologic abnormalities; associated with glomerulonephritis and immune complex disease; associated with immune complex disease without renal disease; associated with anti-GBM antibodies without renal disease; without associated immunologic or renal abnormality. Examples of these disorders are illustrated. Improved clinical-radiographic correlation may lead to earlier diagnosis and treatment of diffuse pulmonary hemorrhage and its causes.
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PMID:Diffuse pulmonary hemorrhage: a review and classification. 315 69

184 cases of acute poststreptococcal glomerulonephritis were investigated and six of these were associated with a peculiar, uncommon pneumonia, and another one had a lethal course. The clinicoradiological and especially pathological data summarized in this study attempt to demonstrate the individuality of this type of pneumonia. Pneumonia associated with acute poststreptococcal glomerulonephritis is similar or identical to rheumatic pneumonia. In both entities, pneumonia and pulmonary edema may and do coexist, and the differentiation of pneumonia from congestive heart failure is difficult and often impossible without pathological evidence. The most attractive pathogenic interpretation is the hypothesis of an immune mechanism in the induction of pneumonia. Authors attributed the lung changes, consecutive to a vascular damage, to a hypersensitivity phenomenon, with accumulation of fibrinogen in alveoli where it is converted to fibrin. Then, the hyaline membrane lining the alveoli, an important feature of pneumonia associated with glomerulonephritis is built up. It is, however, plausible that the effect of the immune reaction is associated with those of hydrosaline retention, arterial hypertension and congestive heart failure. Analogous to rheumatic pneumonia, the "peculiar pneumonia" associated with acute poststreptococcal glomerulonephritis should be named nephritic pneumonia.
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PMID:Uncommon pneumonia associated with acute poststreptococcal glomerulonephritis. 621 50

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

Twenty patients with rapidly progressing glomerulonephritis (RPGN) aged 16-50 underwent plasmapheresis (PA) as adjuvant to immunodepressants. Of these, 9 patients had lupus, 4 Bright RPGN, 4 and 3 patients combined glomerulonephritis with hemorrhagic vasculitis and Wegener granulomatosis, respectively. A total of 130 procedures were performed (3-13 per each patient). The results of PA treatment included complete recovery of renal function in 8 and partial in 10 patients (3 of them could stop hemodialysis), death of pulmonary edema (2 cases). The authors think advisable to combine immunodepressants with PA, especially when the drugs are contraindicated, in patients with malignant glomerulonephritis.
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PMID:[Plasmapheresis in the treatment of rapidly progressing glomerulonephritis]. 837 42

To develop criteria for determining predisposition to pulmonary edema in patients with glomerulonephritis, clinical, laboratory and X-ray examinations were made in 697 patients with glomerulonephritis at different stages of its development. X-ray examination included chest tele X-ray and its densitometric analysis. Twenty two patients underwent computerized tomography with histographic analysis. In 106 patients, X-ray findings were compared with the volume of circulating blood, cardiac and stroke indices. Changes in the lungs and pleural cavities were found in 22.7%, pulmonary edema was revealed in 15.7% of the patients. The prognostically unfavourable criteria for the development of pulmonary edema were found to be Stage II pulmonary venous hypertension with hypervolemia and peripheral edemas. The densitometrically detected increase in the density of the lower lungs in patients with Stage II venous hypertension suggests early manifestations of interstitial edema of the lung and the narrowing of the histogram angle limited by its ascending and descending lines is indicative of the fact that interstitial edema progresses to alveolar one.
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PMID:[The x-ray diagnosis of a predisposition to nephrogenic pulmonary edema in glomerulonephritis patients]. 875 10

A newly identified intraerythrocytic Babesia-like organism, WA1, and its relatives were recently shown to be infectious for humans in the western United States. The purpose of the present study was to determine the susceptibilities of selected mouse genotypes to WA1 infection in an attempt to develop a murine model of the human disease. Several mouse strains were inoculated intraperitoneally with various passages of WA1-parasitized erythrocytes. Parasitemia was evaluated by blood smears and by PCR with blood samples collected at various intervals after inoculation. Hematologic parameters were monitored in blood samples at all intervals. C57BL/6 and C57BL/10 mice exhibited mortality rates of <10%. BALB/cJ, CBAJ, and 129/J mice had higher peak parasitemias than did C57BL mice, with mortality rates of 40, 50, and 50%, respectively. A/J, AKR/N, C3H, and DBA/1J mice also had higher peak parasitemia and mortality rates (>95%). An F1 cross of C57BL/6 (resistant) and C3H.RKK (susceptible) mice had a mortality rate similar to that of the resistant parental strain. Histopathology of BALB/cJ and C3H mice at 9 and 14 days after inoculation revealed erythrophagocytosis and deposition of an iron-negative pigment in multiple organs. Morbidly ill C3H mice at 14 days had severe pulmonary edema, hemoglobinuria, and glomerulonephritis.
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PMID:Differential effects of infection with a Babesia-like piroplasm, WA1, in inbred mice. 945 1

The present study was designed to investigate the role of cytokines in the pathogenesis of Babesia caballi in experimentally infected horses. The expression of cytokine mRNA was determined by using reverse transcription-polymerase chain reaction in two B. caballi-infected horses for 2 weeks after the infection. In one horse, there was up-regulation of interferon-gamma, tumor necrosis factor-alpha (TNF-alpha) and interleukin-2 mRNAs, while in the second horse, expression of only TNF-alpha mRNA was up-regulated. No change was observed in interleukin-4 mRNA in both of the horses. To know the relation between nitric oxide (NO) production and pathogenesis, NO production was assayed in three dexamethasone treated-B. caballi-infected horses. Production of NO in all 3 horses increased significantly before death, although the parasitemia level remained very low. Treatment with NO inhibitor resulted in the suppression of NO production and increased parasitemia level in a horse, which died of the infection. The pathological examination showed that the main cause of the death was dyspnoea and pulmonary edema. Histopathologically, diffuse global mesangial proliferative glomerulonephritis was also observed. These results suggested that NO may be a critical effector molecule of immune defense against parasite. TNF-alpha and NO might be contributing to the pathogenesis in B. caballi infection.
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PMID:Pathogenesis of Babesia caballi infection in experimental horses. 981 67


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