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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Wegener's granulomatosis is a necrotizing, granulomatous vasculitis. It usually causes sinusitis, pneumonitis and glomerulonephritis. The common ocular manifestations include conjunctivitis, scleritis, peripheral keratitis and orbital inflammation. We report the case of a 50-year-old woman with Wegener's granulomatosis and very severe ocular complications who underwent bilateral enucleation. The pathologic findings of the eyeballs revealed granulomatous necrotizing scleritis, perivasculitis and granulomatous choroiditis. The last, as far as we know, has not yet been reported.
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PMID:Choroidal involvement in Wegener's granulomatosis: a case report. 974 68

A 61-year-old male was referred to our hospital for rapidly progressive azotemia. He was also found to have huge vegetation at the aortic valve causing regurgitation. Biochemical examinations revealed the presence of an immunocomplex associated with decreased circulating complements. In biopsy samples from the kidney, we found the presence of fibrillar crescents, proliferation of mesangial cells, increase in extracellular matrix proteins, atrophy of tubules, infiltration of mononuclear cells in the interstitial regions, high density deposits in the mesangial area and mesangial interposition. Since the patient strongly rejected operative treatment by valvular replacement, we continued non-invasive treatment such as hemodialysis and treatment with penicillin G. This transiently improved the condition of the patient, including biochemical data and cardiac function, but there was no reduction in the size of vegetation at the aortic valve and the bacteria responsible for infective endocarditis were not identified. About three months after admission, overt signs of congestive heart failure emerged and the patients was subjected to intensive care with a respirator and hemodynamic monitoring. Although the cardiac function was improved, concomitant severe pneumonia occurred and the patient died of septic shock. Thus, we report a rare case in whom immune complex-mediated glomerulonephritis was associated with infective endocarditis with aortic valve vegetation.
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PMID:[Immune complex-mediated glomerulonephritis associated with infective endocarditis with aortic valve vegetation]. 975 94

Infections are one of the major causes of morbidity and mortality during the course of systemic lupus erythematosus, and are promoted by various dysfunctions of the immune system, some of which are poorly understood. Other predisposing factors have been also identified such as the presence of glomerulonephritis and a treatment with high-dose corticosteroids or immunosuppressors. These factors have been particularly associated with the occurrence of opportunistic infections such as systemic candidiasis or Pneumocystis carinii pneumonia, whose frequency has increased with the intensity of therapeutic strategies. The most frequent infections encountered are induced by community-acquired microorganisms. Thus, initiating an empirical antibiotic treatment is justified in febrile patients with lupus erythematosus. In case of marked lymphopenia, it is recommended to start cotrimoxazole as primary prophylaxis against P. carinii pneumonia.
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PMID:[Infections and lupus]. 978 Nov 35

Antiglomerular basement membrane (anti-GBM) disease is characterized by a linear deposition of immunoglobulins along the glomerular basement membrane. A 67-year-old man with a recently discovered monoclonal gammopathy of unknown significance (MGUS) presented with microscopic hematuria, nephrotic-range proteinuria, and rapidly deteriorating renal function after a pneumonia. Renal histology showed a crescentic glomerulonephritis; immunohistology showed intense linear staining of the GBM with immunoglobulin A (IgA) and moderate linear staining with kappa and lambda light chains. Screening for systemic disease, including diabetes mellitus, lupus erythematodes disseminatus, cryoglobulinemia, was negative. Serological tests for detection of anti-GBM antibodies were positive for IgA class and negative for IgG. Further examination indicated a bronchial carcinoma T2N2M0. This clinical report adds new information to the spectrum of anti-GBM disease and suggests that neoplasia may be associated with unusual exposure of and/or immune response to epitopes in the GBM.
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PMID:IgA antiglomerular basement membrane disease associated with bronchial carcinoma and monoclonal gammopathy. 1007 3

A three-year-old weimaraner was presented with lethargy, anorexia, neck pain and a soft fluctuant swelling in the thoracic inlet. A cough had been noted previously. Clinical examination revealed tachycardia, tachypnoea, pallor and a large subcutaneous swelling, with bruising, suggestive of a haematoma in the thoracic inlet. Thoracic radiographs revealed a cranial mediastinal mass which had the ultrasonographic appearance of fluid, and there was also a marked generalised interstitial lung pattern. Routine haematology revealed severe anaemia and thrombocytopenia, although coagulation tests were within normal limits. A diagnosis of immune-mediated thrombocytopenia was however made on the basis of a positive antiplatelet antibody test and a rapid response to prednisolone therapy. Furthermore, a tentative diagnosis of Angiostrongylus vasorum infection was suggested on the basis of clinical and radiographic findings, although no lungworm larvae were identified on faecal analysis. Despite initiating treatment with fenbendazole, the dog died suddenly. Postmortem examination revealed myocarditis, thrombosing arteritis, pneumonia and chronic membranoproliferative glomerulonephritis associated with A vasorum infection.
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PMID:Immune-mediated thrombocytopenia associated with Angiostrongylus vasorum infection in a dog. 1038 68

The combination of hemorrhagic pneumonitis and rapidly progressive glomerulonephritis is a characteristic feature of Goodpasture's syndrome (GPS), an autoimmune disease resulting from the interaction of pathogenic anti-collagen type IV (C-IV) antibodies with alveolar and glomerular basement membranes. Lack of a suitable animal model for this fatal disease has hampered both a basic understanding of its etiology and the development of therapeutic strategies. We now report a novel model for GPS using mice deficient in a central regulatory receptor for immunoglobulin (Ig)G antibody expression and function, the type IIB Fc receptor for IgG (FcgammaRIIB). Mutant mice immunized with bovine C-IV reproducibly develop massive pulmonary hemorrhage with neutrophil and macrophage infiltration and crescentic glomerulonephritis. The distinctive linear, ribbon-like deposition of IgG immune complex seen in GPS was observed along the glomerular and tubulointerstitial membranes of diseased animals. These results highlight the role of FcgammaRIIB in maintaining tolerance and suggest that it may play a role in the pathogenesis of human GPS.
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PMID:Fcgamma receptor IIB-deficient mice develop Goodpasture's syndrome upon immunization with type IV collagen: a novel murine model for autoimmune glomerular basement membrane disease. 1070 70

We describe two patients with sarcoidosis with lesions of granulomatous interstitial nephritis (GIN) and postinfectious glomerulonephritis (GN). Both patients presented with heavy proteinuria, hematuria, and renal failure. Renal histology in both showed GIN and glomerular changes of proliferative GN with hump-like subepithelial deposits by electron microscopy of postinfectious GN. Antecedent history of pneumonia was present in one, and ASO titer was elevated in the other. The proteinuria and azotemia improved in both with steroid therapy. Reports of "postinfectious" or diffuse proliferative GN in patients with sarcoidosis are rare. The authors are unaware of reports of concomitant sarcoid GIN and postinfectious GN. Although acute renal insufficiency or failure can occur with GIN or other more common renal lesions primary glomerular disease should be considered in patients with sarcoidosis who present with renal dysfunction. This is a US government work. There are no restrictions on its use.
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PMID:Renal sarcoidosis with superimposed postinfectious glomerulonephritis presenting as acute renal failure. 1087 3

A 58-year-old man developed proteinuria and renal dysfunction following pneumonia caused by methicillin-resistant Staphylococcus aureus (MRSA). Vancomycin was administered, and prednisolone pulse therapy and plasmapheresis were performed. Subsequently, serum creatinine was decreased. Eight months later, creatinine and CRP were again elevated, and MRSA was detected. Vancomycin was again administered and plasmapheresis was performed. However, renal function was not improved and continuous hemodialysis was initiated. This case indicates that complete eradication of MRSA is necessary to treat MRSA-associated glomerulonephritis, and if this is not attained, a permanent loss of renal function occurs.
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PMID:Glomerulonephritis after methicillin-resistant Staphylococcus aureus infection resulting in end-stage renal failure. 1139 3

Microscopic polyangiitis is a very rare disease characterized by the lesions of arteriolae, venulae and capillaries--mainly of the kidneys and lungs, but also of other systems and organs. The elevated titer of anti-myeloperoxidase ANCA is very important immunological indicator. The main changes in our patient were related to the lung bleeding and rapidly progressive glomerulonephritis. The treatment has started according to the standard Fauci scheme adjusted to the level of disease severity and the age of patient (prednisone 60 mg/24 h, along with the gradual dosage decrease, cyclophosphamide 150 mg/24 h) and has lead to the clinical-laboratory remission. The patient had the leukocyte values irregularly controlled during the immunosuppressive therapy and agranulocytosis thus caused was not spotted in time, leading to the inadequate treatment of pneumonia that brought on the lethal outcome.
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PMID:[Microscopic polyangiitis]. 1154 60

We report an autopsy case of elderly-onset anticentromere antibody-positive pulmonary-renal syndrome. An 84-year-old woman was admitted to our hospital with complaints of leg edema and general malaise. Neither skin rush nor arthritis was seen. Because of hematuria, proteinuria with various casts, renal dysfunction and anemia, a clinically diagnosis of rapidly progressive glomerulonephritis was made. Slight pulmonary hypertension was observed in ultrasonic cardiography. Hypocomplementemia was not seen. Tests for MPO- and PR 3-anti-neutrophil cytoplasmic antibodies and anti-glomerular basement membrane antibody were negative, but a high titer of antinuclear antibody with a discrete speckled pattern on immunofluorescent staining was disclosed. Results for anticentromere antibody and anti-Ki antibody were positive, but for anti-Sm antibody and anti-double stranded DNA antibody were both negative. She did not present any clinical features of systemic sclerosis or CREST syndrome. Subsequently, prednisolone was administered, but pulmonary alveolar hemorrhage occurred and the patient died of acute respiratory failure caused by massive pulmonary hemorrhage. Autopsy revealed crescentic glomerulonephritis including glomerular capillaritis and pulmonary capillaritis with positive granular deposits of immunoglobulins and compliment on the glomerular and pulmonary capillary walls. Immunologically mediated crescentic glomerulonephritis and pulmonary capillaritis was then diagnosed histopathologically. The main pathological feature of the case was small-vessel vasculitis with immune-complex deposition. Although this case did not fulfill the clinical criteria for systemic lupus erythematosus (SLE), its histological features resembled those of lupus nephritis and acute lupus pneumonitis. We speculated that anticentromere antibody-positive pulmonary-renal syndrome without any other symptoms or signs of connective tissue disease, such as our case, is a clinical entity distinct from typical SLE or CREST syndrome.
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PMID:[Elderly-onset anticentromere antibody-positive pulmonary-renal syndrome: report of an autopsy case]. 1157 30


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