Tubular dilatation in the repair process of ischaemic tubular necrosis.
To elucidate the mechanisms of renal tubular dilatation in acute tubular necrosis (ATN), morphological findings after 60 min ischaemia were studied in rats. The characteristics of the tubular basement membrane (BM) were also examined. A morphometric analysis of cell proliferation, epithelial cellularity and the circumference of damaged tubules was performed. The ischaemic injury resulted in widespread necrosis of renal tubules at day 1, and the BM of damaged tubules appeared thin. The intensity of the immunohistochemical staining for BM components decreased. The epithelial cell proliferation was particularly active in the early phase. Dilatation of the damaged tubules began at day 2, and the degree of dilatation increased up to day 6. Regenerative epithelial hyperplasia occurred and abnormalities of tubular BM were seen. Epithelial hyperplasia and dilatation of damaged tubules was most prominent at day 6 and the tubular BM was thickened by newly produced BM components. Tubular obstruction was not seen and tubules returned to normal size by day 28. Epithelial hyperplasia and abnormalities of tubular BM disappeared progressively. Regenerative tubular epithelial hyperplasia and abnormalities of tubular BM may play an important role in pathogenesis of tubular dilatation in ATN, and tubular dilatation is not due to tubular obstruction.
Shimizu
A
A
Department of Pathology, Nippon Medical School, Tokyo, Japan.
Masuda
Y
Y
Ishizaki
M
M
Sugisaki
Y
Y
Yamanaka
N
N
D000818:Animals; D001485:Basement Membrane / Q000648:ultrastructure; D002455:Cell Division; D004195:Disease Models, Animal; D007091:Image Processing, Computer-Assisted; D007511:Ischemia / Q000473:pathology*; D007668:Kidney / Q000098:blood supply*; D007683:Kidney Tubular Necrosis, Acute / Q000473:pathology*; D007684:Kidney Tubules / Q000473:pathology*; D008297:Male; D008854:Microscopy, Electron; D051381:Rats; D017208:Rats, Wistar