Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five consecutive patients with well-documented Goodpasture's syndrome were treated with plasmapheresis and immunosuppression. In all patients, the antiglomerular basement-membrane antibody titers decreased with treatment. In three patients, hemoptysis responded promptly to plasmapheresis. Two patients presenting with severe renal failure required chronic dialysis, and three patients who had serum creatinine levels less than 2.1 mg/dl before treatment improved or had stabilization of their renal function. We confirm that the use of plasmapheresis and immunosuppression is a promising method of treatment in some patients with Goodpasture's syndrome.
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PMID:Use of combined plasmapheresis and immunosuppression in the treatment of Goodpasture's syndrome. 49 63

A 38-year-old man was hospitalized for proteinuria, and pitting edema. He had noticed Raynaud's phenomenon at about age fifteen. One month prior to admission, his urine contained protein and the serum creatinine was 3.0 mg/dl. On admission, sclerodactylia, digital pitting scar of fingertips, digital bone absorption and pulmonary fibrosis were observed and a diagnosis of progressive systemic sclerosis (PSS) was made. Laboratory investigations revealed: 24-hour urine protein excretion 3 g; serum creatinine 5.6 mg/dl; creatinine clearance 13.5 ml/min; antinuclear factor strongly positive in a speckled pattern; antibodies to nRNP positive with a titer of 1: 20, 480; antibodies to DNA, Sm, SS-A, SS-B, Scl-70, centromere and Jo-1 negative; serum complement normal. A renal biopsy revealed focal and segmental necrotizing glomerulonephritis with 70% crescents but no vascular changes. Circulating antiglomerular basement membrane antibodies were negative. Immunofluorescence disclosed granular deposits of IgM and C3 in the mesangium and along the capillary walls. Treatment was begun with methylprednisolone pulse therapy. After 5 month, serum creatine and creatinine clearance were 1.9 mg/dl and 35 ml/min, respectively. A year after the discharge, he was readmitted for hemoptysis and worsening of proteinuria and microhematuria. A chest radiograph demonstrated bilateral alveolar consolidation. Serum creatinine was elevated to 3.5 mg/dl. The continuous hemoptysis resulted in a severe dyspnea associated with a rapid fall in the hemoglobin. On the fourth hospital day, the PaO2 was 41 Torr on oxygen by mask that necessitated mechanical ventilation and pulse therapy was started. However, the patient died on the ninth hospital day of respiratory failure due to pulmonary hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of progressive systemic sclerosis complicated by crescentic glomerulonephritis and diffuse pulmonary hemorrhage]. 147 23

We report the case of a 39-year-old male patient with Goodpasture's syndrome. Despite therapy with prednisone, cyclophosphamide and plasma exchanges, serum creatinine (Scr) progressively increased up to 10.3 mg/dl (936 mumol/l) and hemoptysis recurred 3 months after initiation of treatment. Ciclosporin (CS) starting at 6 mg/kg/day was given. Scr began to decrease 2 weeks later and eventually stabilized at approximately 2.0 mg% (182 mumol/l). This case illustrates one of the potential uses of CS in human glomerular disease.
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PMID:Ciclosporin in Goodpasture's syndrome. 156 89

Fourteen cases of anti-GBM antibody-induced RPGN were evaluated retrospectively in terms of renal function improvement and therapeutic risks. Nine men and 5 women (mean age: 55.3 years) were observed over a 9 year period; in three patients, hemoptysis was associated with renal disease (Goodpasture's syndrome). Most of these patients had received combinations of steroid therapy (ST), immunosuppressive drugs (IS) and plasma exchanges (PE). Age, duration of symptoms prior to diagnosis, initial renal function, therapeutic modalities and complications were assessed according to renal outcome: 9 patients (group A, "non-responders") remained on dialysis irrespective of the treatment administered; 5 patients (group B, "responders") recovered renal function. Complications, especially infections, were twice as frequent in group A. Two of the 4 recorded deaths were related to the disease or the treatment. Analysis of clinical and pathological values at the time of entry into the study for both groups indicated that oliguria/anuria, serum creatinine greater than 500 mumol/l and greater than 50% crescents, when associated, were factors predictive of poor renal outcome; in these patients, dialysis may be required except in cases of pulmonary hemorrhage. In all other patients, treatment with ST, IS and PE is recommended. Active hemoptysis necessitates pulse steroids or PE; if absent, further tests (carbon monoxide uptake, bronchoalveolar lavage, lung biopsy) are indicated before use of aggressive therapy.
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PMID:[Anti-basement-membrane antibody mediated, rapidly progressive, glomerulonephritis. Diagnostic and therapeutic strategy based on a retrospective study of 14 cases]. 225 83

27 cases of uremia with abnormal appearances on the chest films were analysed. The results showed that the clinical features were cough, expectoration dyspnea and hemoptysis. However, the degree of these symptoms was relatively mild as judged from the amount of pulmonary edema found on the chest films. The chest X-ray finding in these group of patients were characterized by pulmonary blood stasis, interstitial edema of the lung and edematous alveoli. The pathogenesis of uremic lung was said to be related to blood urea nitrogen and creatinine retention and the concurrent presence of left side heart failure may also play a role. Hemodialysis and other comprehensive treatments could help the patients with uremic lung for relief the symptoms. But the fundamental managements to improve the prognosis for this disease are early treatment of the primary renal diseases, in order to prevent the occurrence of renal failure. Kidney transplantation should be advised.
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PMID:[The uremic lung]. 263 29

A young woman presented with arthralgia, a rash and dramatic haemoptysis, and renal involvement was indicated by proteinuria, haematuria and a rising serum creatinine. A systemic vasculitic disorder was suspected initially, but the diagnosis of Henoch-Schonlein purpura was established by the finding of mesangial IgA deposits on renal biopsy. Immunofluorescent study of renal biopsy material is vital to diagnosis where the clinical features of Henoch-Schonlein purpura and those of the systemic vasculitides with renal involvement prove to be indistinguishable.
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PMID:Henoch Schonlein purpura presenting with pulmonary haemorrhage. 356 74

The aetiology, clinical features and outcome of 40 patients presenting with Goodpasture's syndrome (glomerulonephritis with haemoptysis and pulmonary infiltrates) are reviewed. The diseases of the patients studied could be divided into three groups: antiglomerular basement membrane (anti-GBM) antibody-induced disease (7/40); systemic vasculitis (22/40) and idiopathic Goodpasture's syndrome (i.e. no systemic disease or anti-GBM antibody detected) (11/40). Overall mortality was 57.5 per cent (anti-GBM disease 4/7; systemic vasculitis 15/22; and idiopathic Goodpasture's syndrome 4/11). Most patients died of disease progression or infection. End-stage renal failure developed in 26 patients (anti-GBM (7), vasculitis (14) and idiopathic Goodpasture's syndrome (5). End-stage renal failure developed in 23 of 24 patients presenting with a creatinine of greater than 600 microM/l regardless of the aetiology of Goodpasture's syndrome or treatment used. Review of renal histology showed that all had proliferative nephritis, with 80 per cent of patients having more than 30 per cent crescents. Thus Goodpasture's syndrome was associated with a wide variety of underlying disease. It had a poor prognosis, with the degree of renal impairment at presentation, the extent of crescent formation and the nature of the underlying disease being the major determinants of outcome.
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PMID:The clinical spectrum of acute glomerulonephritis and lung haemorrhage (Goodpasture's syndrome). 401 44

We report two cases with Goodpasture's syndrome successfully treated by membrane plasma exchange. In both patients, pulmonary infiltrations and hemoptysis had already resolved after the first pulse methylprednisolone dose (1000 mg IV). Following plasma exchange, renal function did not further deteriorate in one patient and returned to normal in the other patient. From the clinical course of our patients and a review of the literature, we conclude that membrane plasma exchange is effective in preventing deterioration of renal function in Goodpasture's syndrome. Analysis of the literature shows that patients who respond to plasma exchange have significantly fewer crescents and lower plasma creatinine, while non-responders are more often oliguric or anuric and require dialysis at the time of plasma exchange.
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PMID:Membrane plasma exchange in Goodpasture's syndrome. 673 78

A 62-year-old man was admitted to our hospital because of low-grade fever and hemoptysis. Chest roentgenogram revealed diffuse infiltrative shadows with air bronchograms. Bronchoalveolar lavage fluid demonstrated bloody fluid, including many hemosiderin-laden macrophages. In addition, his laboratory data on admission revealed elevation of serum creatinine and BUN, and proteinuria and hematuria on urinalysis. Renal needle biopsy showed atrophic glomeruli and mesangial proliferative glomerulonephritis without crescent formation. A history of wheezing and slight eosinophila was also present, and we therefore suspected allergic granulomatous angitis. We performed airway sensitivity and reversibility tests, which were positive, and so we judged that he had an asthmatic component. Perinuclear antineutrophil cytoplasmic antibody (P-ANCA) was positive (x 1000) with ELISA. We diagnosed diffuse alveolar hemorrhage with mesangial proliferative glomerulonephritis and bronchial asthma. His general condition improved with oral administration of corticosteroid (50 mg/day) and immunosuppressive agent (cyclophosphamide; 50 mg/day), and his major symptoms disappeared within a few days.
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PMID:[A case of diffuse alveolar hemorrhage accompanied by mesangial proliferative glomerulonephritis with positive perinuclear anti-neutrophil cytoplasmic antibody]. 780 59

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


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