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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and histological features of 43 patients with rapidly progressive glomerulonephritis were reviewed. All had extensive crescent formation in more than 50 per cent of glomeruli. Three distinct patterns of immunofluorescent staining were identified: linear, granular, and sparse staining. Electron microscopy was valuable in corroborating the results of immunofluorescence. The prognosis was poor, with no patient regaining normal renal function regardless of treatment. Significant differences were observed among patients categorized by immunofluorescent staining. Those with a linear pattern were younger and more commonly had hemoptysis. Patients with sparse immunofluorescent staining had better renal function at the time of presentation and a longer duration of illness.
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PMID:Rapidly progressive glomerulonephritis in adults: clinical and histologic correlations. 69 99

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 a case of a 53-year-old woman diagnosed of systemic sclerosis. She underwent an episode of pulmonary haemorrhage, characterized by haemoptysis, sudden anaemization, and bilateral alveolar infiltration during her hospitalization, which was resolved with steroid treatment. Subsequently, she developed a focal necrotizing glomerulonephritis. After searching in the literature, we have found only three cases of systemic sclerosis associated with pulmonary haemorrhage. We discuss the etiopathogenesis of this association and stress the importance of early steroid therapy.
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PMID:Pulmonary haemorrhage and focal necrotizing glomerulonephritis in a case of systemic sclerosis. 158 10

We report a case of idiopathic crescentic glomerulonephritis with pulmonary hemorrhage associated with anti-myeloperoxidase antibodies (anti-MPO ab). A 74 year-old female was admitted to our hospital because of rapidly progressive glomerulonephritic syndrome and dyspnea with bloody sputum. On admission anti-MPO ab, one of anti-neutrophil cytoplasmic antibodies, were detected but anti-GBM antibodies and immune complexes were not detected. Renal biopsy showed crescentic glomerulonephritis and lung biopsy showed massive alveolar hemorrhage. Both tissue had pauci-immune deposit by immunofluorescence microscopy. Hemodialysis and steroid administration were started. Pulmonary hemorrhage was improved remarkably, but renal failure progressed rapidly to end stage kidney, then hemodialysis was continued. Although subsequent 3 years uneventful maintenance hemodialysis had been performed, she admitted to our hospital again because of progressive dyspnea with hemoptysis after upper respiratory tract infection. On admission anti-MPO ab were detected again and steroid administration was started. Pulmonary hemorrhage was improved with decreased anti-MPO ab titer. While tapering the dosis of steroid, anti-MPO ab again increased and pulmonary hemorrhage recurred. Although pulse methylprednisolone therapy and plasma exchange were performed, respiratory failure progressed rapidly and she died of sepsis. Postmortem examination showed no evidence of systemic vasculitis. In this case, titer of anti-MPO ab was associated with not only idiopathic crescentic glomerulonephritis but also with pulmonary hemorrhage. We tried to detect enzymatically active MPO in serum. Titer of serum MPO was also associated with disease activity and anti-MPO ab. It is suggested that both anti-MPO ab and serum MPO are closely related to the pathogenesis of idiopathic crescentic glomerulonephritis and pulmonary hemorrhage.
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PMID:[A case of anti-myeloperoxidase antibodies-associated idiopathic crescentic glomerulonephritis with pulmonary hemorrhage]. 166 75

The value of antineutrophilic cytoplasmic antibodies (ANCA) was assessed in the diagnosis and chronic treatment of 7 patients with microscopic polyarteritis or Wegener's granulomatosis. All patients had oligoimmune glomerulonephritis with segmental and focal necrosis and presented with anaemia. Five of them had alveolar haemorrhage with haemoptysis and infiltrates at radiography. ANCA were assayed by indirect immuno-fluorescence on ethanol-fixed neutrophils and were strongly positive, with a cycloplasmic aspect in 5 cases and a perinuclear aspect in 2 cases. Initial remission with fall in ANCA titres was obtained with corticosteroids, cyclophosphamide and sometimes plasmapheresis (5 patients), but frequent relapses with re-elevation of ANCA titre occurred when treatment was reduced. It is concluded that ANCA are very helpful in the diagnosis of systemic vasculitis, notably in cases with first-time alveolar haemorrhage. They also facilitate monitoring and therapeutic decisions, since relapses are frequent.
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PMID:[Alveolar hemorrhage, glomerulonephritis and anti-cytoplasmic polynuclear antibodies]. 175 66

A 76 year old white woman died from massive pulmonary haemorrhage nine days after she was admitted to Parkland Memorial Hospital for evaluation of haemoptysis and rapidly progressive glomerulonephritis. The differential diagnosis of haemoptysis with rapidly progressive glomerulonephritis is presented with particular emphasis on Wegener's granulomatosis and microscopic polyarteritis. Necropsy showed a small vessel necrotising vasculitis associated with a focal segmental necrotising glomerulonephritis consistent with microscopic polyarteritis.
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PMID:Microscopic polyarteritis: a forgotten aetiology of haemoptysis and rapidly progressive glomerulonephritis. 196 38

We describe the clinical course and morphologic findings of a 22-year-old woman presenting with a systemic disease that included nasal ulceration, hemoptysis and rapidly progressive renal failure. Biopsies of nasal septum and lung revealed small vessel leukocytoclastic angiitis while renal biopsy showed a diffuse crescentic glomerulonephritis. Immunosuppressive therapy resulted in remission of clinical symptoms and resolution of glomerulonephritis as documented in a followup biopsy. Although her clinical presentation with triad organ involvement strongly suggested Wegener's granulomatosis, this case illustrates that other varieties of vasculitis may mimic Wegener's granulomatosis.
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PMID:Pulmonary-renal syndrome with "triad" involvement due to small vessel vasculitis. 221 85

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

The case of a patient who presented clinically with hemoptysis and was shown to have bilateral pulmonary infiltrates and renal abnormalities is described. This typical clinical setting was initially diagnosed as Goodpasture's syndrome. Open biopsies of lung and kidney were performed. Light microscopy failed to demonstrate the renal abnormalities most often associated with Goodpasture's syndrome. Immunofluorescence and electron microscopic findings were compatible with a diagnosis of immune complex glomerulonephritis. No immunologic lesions were demonstrated by lung biopsy. Antiglomerular basement membrane antibodies were not detected in the patient's serum. In view of the drastic prognostic and therapeutic consequences of Goodpasture's syndrome, it is essential that this diagnosis be confirmed by tissue examination and serologic testing.
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PMID:Intrapulmonary hemorrhages and immune complex glomerulonephritis masquerading as Goodpasture's syndrome. 294 55

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


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