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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
|
| pubmed:dateCreated |
1995-12-6
|
| pubmed:abstractText |
Renal biopsies from 20 patients with IgAN were retrospectively studied using monoclonal antibodies against T cells, monocytes/macrophages (MM), HLA-DR-related antigen and the C5b-9 neoantigen. Glomerular C5b-9 deposits were mainly found in the mesangial areas and showed an association with IgA (P < 0.005) and C3 deposits (P < 0.001). Interstitial T cells and MM were highly correlated with the interstitial DR + ve cells (P < 0.001 and P < 0.0005 respectively). Tubular C5b-9 deposition was observed on the tubular basement membranes and related to the numbers of interstitial T cells (P < 0.005), MM (P < 0.005) and DR + ve cells (P < 0.01) as well as to the tubular DR expression (P < 0.025). The severity of tubular atrophy and interstitial fibrosis showed a positive correlation with the interstitial T cells, MM and DR + ve cells, as well as with the intensity of tubular C5b-9 deposition (P < 0.05 and P < 0.05 respectively). Plasma creatinine on presentation was correlated with the numbers of interstitial T cells (P < 0.05), MM (P < 0.01), interstitial DR + ve cells (P < 0.005), and tubular C5b-9 deposits (P < 0.005). No correlation between glomerular T cells, MM, and C5b-9 deposits with plasma creatinine was seen. During follow-up, renal function deteriorated in those patients with the more extensive tubular C5b-9 deposits. In conclusion, glomerular C5b-9 deposition seems to be secondary to the IgA and C3 deposition. In contrast, tubular C5b-9 is related to the numbers of interstitial T cells and MM. Activated interstitial mononuclear cells may lead to the tubular deposition of C5b-9, which eventually might contribute to the development of tubulointerstitial lesions (TIL) and renal function impairment.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:issn |
0931-0509
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
10
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1166-72
|
| pubmed:dateRevised |
2004-11-17
|
| pubmed:meshHeading |
pubmed-meshheading:7478119-Adult,
pubmed-meshheading:7478119-Atrophy,
pubmed-meshheading:7478119-Complement Membrane Attack Complex,
pubmed-meshheading:7478119-Creatinine,
pubmed-meshheading:7478119-Female,
pubmed-meshheading:7478119-Fibrosis,
pubmed-meshheading:7478119-Follow-Up Studies,
pubmed-meshheading:7478119-Glomerulonephritis, IGA,
pubmed-meshheading:7478119-Humans,
pubmed-meshheading:7478119-Kidney Glomerulus,
pubmed-meshheading:7478119-Kidney Tubules,
pubmed-meshheading:7478119-Male,
pubmed-meshheading:7478119-Middle Aged
|
| pubmed:year |
1995
|
| pubmed:articleTitle |
The pathogenetic significance of C5b-9 in IgA nephropathy.
|
| pubmed:affiliation |
Department of Nephrology, Aristotelian University of Thessaloniki, Hippokration General Hospital, Greece.
|
| pubmed:publicationType |
Journal Article
|