Research Abstract |
In 1997, we established the database containing clinical laboratory data at the time of renal biopsy, renal histological changes and prognosis of 600 children from 800 renal biopsied cases. Among the chronic renal diseases discovered by annual urine screening examination at school, IgA nephropathy takes 48% by the most, congenital renal anomalies and thin basement membrane disease (TBM) follows 3.1% and 2.2%, respectively. Although urine screening at school is useful for discovering chronic glomeruloneohritides, especially for IgA nephropathy, TBM and hereditary nephritis, there is a limitation in discovery of renal diseases which need infant urinalysis or image analysis for diagnosis, such as congenital renal anomalies and reflux nephropathy. In 1998, Renal expression of alpha chain subclass of type IV collagen protein was examined in 13 children with thin basement membrane disease (TBMD) using deparaffinized sections. Although there was no cases who suffered from renal dysfunction durin
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g 6.1 years' follow-up, one male patient who showed a decreased expression of type IV collagen α 3, 4, and 5 chain protein was proved proteinuria later. As a result, immunohistological procedure of type IV collagen subclass might be a useful for discrimination of TBMD and Alport syndrome. In 1999, we examined the relationship among renal IL-6 deposition, urinary IL-6 excretion and renal pathological changes of IgA nephropathy in 12 patients. Although the significant correlation between urinary excretion and renal deposition of IL-6 has not been observed, that significant positive correlations both between renal IL-6 expression and proteinuria, and between IL-6 expression and renal pathological lesion have been proved. However, we have not found any correlation between urinary IL-6 level and renal lesion or proteinura. In particular, renal IL-6 expression closely correlated to chronic pathological changes, therefore it will be possible that renal IL-6 overdue expression could be used as a indicator of protracted course of IgA nephropathy. Less
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