Source:http://linkedlifedata.com/resource/pubmed/id/18620732
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
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| pubmed:dateCreated |
2008-9-8
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| pubmed:abstractText |
Little information is available regarding renal histology in cases of chronic allograft dysfunction and graft failure in patients with recurrent immunoglobulin A nephropathy. We compared 57 renal allograft biopsies of 44 patients with recurrent immunoglobulin A nephropathy to 43 biopsies of 33 patients without immunoglobulin A nephropathy recurrence. Clinical parameters such as patient demography and biopsy indications did not differ between the 2 groups, with the exception of time to biopsy. Renal allograft injury, which was assessed by semiquantitative scoring of glomerular, tubulointerstitial, and arteriolar changes, increased linearly over time after transplantation in both recurrent and nonrecurrent samples. Glomerular injuries were significantly correlated with tubulointerstitial injuries in both groups, but the correlation graph reflected an increasing gap in the degrees of tubulointerstitial injury between the 2 groups over time. The levels of glomerulosclerosis, mesangial proliferation, and crescent formation were significantly higher in recurrent samples, whereas the prevalence of chronic rejection was significantly higher in nonrecurrent samples. The presence of segmental sclerosis was associated with significant proteinuria in recurrent samples. Graft survival was better in recurrent immunoglobulin A nephropathy patients than in nonrecurrent patients (74.4% versus 51%) at 10 years after transplantation. In conclusion, slow and progressive glomerular injury is the major cause of long-term graft failure in patients with recurrent immunoglobulin A nephropathy. In contrast, rapidly increasing tubulointerstitial injury is responsible for graft failure in nonrecurrent patients.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II Type 1 Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin-Converting Enzyme...,
http://linkedlifedata.com/resource/pubmed/chemical/Biological Markers,
http://linkedlifedata.com/resource/pubmed/chemical/Methylprednisolone
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| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
1532-8392
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
39
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1511-8
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| pubmed:meshHeading |
pubmed-meshheading:18620732-Adult,
pubmed-meshheading:18620732-Angiotensin II Type 1 Receptor Blockers,
pubmed-meshheading:18620732-Angiotensin-Converting Enzyme Inhibitors,
pubmed-meshheading:18620732-Biological Markers,
pubmed-meshheading:18620732-Biopsy,
pubmed-meshheading:18620732-Disease Progression,
pubmed-meshheading:18620732-Female,
pubmed-meshheading:18620732-Glomerulonephritis, IGA,
pubmed-meshheading:18620732-Graft Rejection,
pubmed-meshheading:18620732-Humans,
pubmed-meshheading:18620732-Kidney,
pubmed-meshheading:18620732-Kidney Glomerulus,
pubmed-meshheading:18620732-Kidney Transplantation,
pubmed-meshheading:18620732-Male,
pubmed-meshheading:18620732-Methylprednisolone,
pubmed-meshheading:18620732-Microscopy, Fluorescence,
pubmed-meshheading:18620732-Postoperative Complications,
pubmed-meshheading:18620732-Proteinuria,
pubmed-meshheading:18620732-Recurrence,
pubmed-meshheading:18620732-Transplantation, Homologous
|
| pubmed:year |
2008
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| pubmed:articleTitle |
Progression of renal allograft histology after renal transplantation in recurrent and nonrecurrent immunoglobulin A nephropathy.
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| pubmed:affiliation |
Department of Pathology, Yonsei University College of Medicine, Seoul 120-752, Korea. jeong10@yumc.yonsei.ac.kr
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| pubmed:publicationType |
Journal Article,
Comparative Study
|