| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Masafumi Jikei Univ., Sch. of Med., Pathology, Lecturer, 医学部, 講師 (70119816)
INOMATA Izuru Jikei Univ., Sch. of Med., Pathology, Lecturer, 医学部, 講師 (30057046)
YAMAGUCHI Yutaka Jikei Univ., Sch. of Med., Pathology, Lecturer, 医学部, 講師 (60057073)
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| Research Abstract |
Tubulo-interstitial lesion(TIL)is often accompanied by glomerular sclerosis in various glomerular diseases,
and its extent is correlated to renal function deterioration. To evaluate the characteristics and histogenesis of TIL in various renal diseases, histopathological analysis by means of lmmunohistochemistry, light and electron microscopy, and morphometry was carried out using renal biopsy specimens obtained from the patients with various renal diseases.
In IgA- and membranoproliferative glomerulonephritis, the extent of TIL was generally much milder than the that of glomerular lesions at the Initial biopsy, and subsequently became wider as glomerular sclerosis progressed. There was a correlation between the extent of TIL and age, suggesting that the vulnerability against Injuries might play a role In tissue. repair In younger generation. However, In focal glomerular sclerosis(FGS), we often found TIL around the segmental lesions at the Initial biopsy, and the TIL was more extensive t
… More
han that observed In other glomerular diseases. The fact suggested that the formation of TIL in FGS could be related with some other factors which are yet to be clarifled. In lupus nephritis, extra-glomerular Immune deposition which was predominant in active state, might be connected with the formation of TIL. In acute tubular necrosis, tubular injuries were often accompanied by the alteration of peritubular capillary walls followed by interstitial edema and inflammatory cellular infiltration. Frequent deposition of Tamm-Horsfall protein in interstitium and venuies suggested of participation of intrarenal reflux. In hemolytic uremic syndrome, the TIL was significantly correlated with glomerular lesions and arteriolar thrombosis, indicating that it was caused by the reduction of postglomerular blood flow. In interstitial nephritis and in acute cellular rejection, the expansion of interstitial spaces was due to high grade inflammatory cell infiltration and edema. "Tubulitis" was pathognomonic in association with tubular epithelial injuries. Tubular atrophy and reduction of peritubular capillary flow might induce TIL. Cytoplasmic interconnection between neighboring interstitial cells formed a network of drainage channel system. The interstitial cells were thought to be capable of transformation into fibroblast/fibrocyte. Less
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