| pubmed-article:3314527 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3314527 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:3314527 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:3314527 | lifeskim:mentions | umls-concept:C0015350 | lld:lifeskim |
| pubmed-article:3314527 | lifeskim:mentions | umls-concept:C0178664 | lld:lifeskim |
| pubmed-article:3314527 | lifeskim:mentions | umls-concept:C0451718 | lld:lifeskim |
| pubmed-article:3314527 | lifeskim:mentions | umls-concept:C0009545 | lld:lifeskim |
| pubmed-article:3314527 | lifeskim:mentions | umls-concept:C1441616 | lld:lifeskim |
| pubmed-article:3314527 | lifeskim:mentions | umls-concept:C0439662 | lld:lifeskim |
| pubmed-article:3314527 | lifeskim:mentions | umls-concept:C2603343 | lld:lifeskim |
| pubmed-article:3314527 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:3314527 | pubmed:dateCreated | 1987-12-9 | lld:pubmed |
| pubmed-article:3314527 | pubmed:abstractText | Renal tissue obtained from 8 patients with reflux nephropathy was studied by immunofluorescence with well-defined mono- and polyclonal antibodies to extracellular matrix, intermediate filament proteins, membrane attack complex of complement (MAC), and immune cells. In both unscarred and scarred areas of the tissue, intrinsic components of the human glomeruli, such as Type IV collagen, laminin, and fibronectin, accumulated in the expanded mesangium of the glomeruli. Those components were diminished or absent in the hyalinized glomeruli. Type III collagen was occasionally localized to the mesangium and synechiae in the glomeruli and was frequently observed within the nearly hyalinized glomeruli. MAC was co-deposited with C3, C5, C9, and properdin in the sclerotic area of the glomeruli, along with a decrease in the reactivity of podocytes with anti-vimentin antibody. Numerous suppressor/cytotoxic T cells were identified in the glomeruli and widened interstitum. Monocytes/macrophages also infiltrated the glomeruli. The present study suggests that accumulation of extracellular matrix, activation of the complement system, and infiltration of suppressor/cytotoxic T cells and monocytes/macrophages are closely associated with the glomerular obsolescence and the progression of reflux nephropathy. | lld:pubmed |
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| pubmed-article:3314527 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:3314527 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:3314527 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3314527 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:3314527 | pubmed:issn | 0002-9440 | lld:pubmed |
| pubmed-article:3314527 | pubmed:author | pubmed-author:MiyamotoHH | lld:pubmed |
| pubmed-article:3314527 | pubmed:author | pubmed-author:YoshiokaKK | lld:pubmed |
| pubmed-article:3314527 | pubmed:author | pubmed-author:MatsubaraKK | lld:pubmed |
| pubmed-article:3314527 | pubmed:author | pubmed-author:MakiSS | lld:pubmed |
| pubmed-article:3314527 | pubmed:author | pubmed-author:TakemuraTT | lld:pubmed |
| pubmed-article:3314527 | pubmed:author | pubmed-author:AkanoNN | lld:pubmed |
| pubmed-article:3314527 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3314527 | pubmed:volume | 129 | lld:pubmed |
| pubmed-article:3314527 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3314527 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3314527 | pubmed:pagination | 223-31 | lld:pubmed |
| pubmed-article:3314527 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:3314527 | pubmed:year | 1987 | lld:pubmed |
| pubmed-article:3314527 | pubmed:articleTitle | Immunohistochemical studies of reflux nephropathy. The role of extracellular matrix, membrane attack complex, and immune cells in glomerular sclerosis. | lld:pubmed |
| pubmed-article:3314527 | pubmed:affiliation | Department of Pediatrics, Kinki University School of Medicine, Osaka, Japan. | lld:pubmed |
| pubmed-article:3314527 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3314527 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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