Genesis of renal tubular atrophy in experimental hydronephrosis in the rat. Role of apoptosis

Gobe, G. C. and Axelsen, R. A. (1987) Genesis of renal tubular atrophy in experimental hydronephrosis in the rat. Role of apoptosis. Laboratory Investigation, 56 3: 273-281.

Author Gobe, G. C.
Axelsen, R. A.
Title Genesis of renal tubular atrophy in experimental hydronephrosis in the rat. Role of apoptosis
Journal name Laboratory Investigation   Check publisher's open access policy
ISSN 0023-6837
Publication date 1987-03
Sub-type Article (original research)
Volume 56
Issue 3
Start page 273
End page 281
Total pages 9
Place of publication London, United Kingdom
Publisher Nature
Language eng
Abstract A morphological study was undertaken to assess the role of cell deletion by apoptosis in experimental hydronephrosis. Male Sprague-Dawley rats (200 ± 20 gm) were used. The left ureter was ligated or a sham operation was carried out. Animals were killed from 4 days to 12 weeks after operation. Two parallel studies were undertaken: one to demonstrate and quantitate specific morphological changes in the affected kidney using light and electron microscopy, and the other to measure changes in dry kidney weights. Renal tubular atrophy is an inevitable consequence of chronic occlusion of the ureter. As expected, the present study showed a progressive loss of tissue mass in the hydronephrotic kidney. This occurred from 1 week after permanent ureteric ligation, and was most rapid between 2 and 4 weeks. The tubular epithelium contained cells undergoing a distinct form of cell death termed apoptosis, characterized ultrastructurally in its early stage by the presence of rounded cells with condensed cytoplasm and condensed and marginated nuclear chromatin, and later by the presence of discrete membrane-bounded intact cellular fragments (apoptotic bodies), which were phagocytosed and digested by adjacent viable cells, or were shed into the tubular lumens. Numbers of apoptotic cells or clusters of apoptotic bodies were increased significantly in all animals with ureter obstruction in comparison with controls. The greatest increases occurred at 2 and 4 weeks, when loss of renal mass was occurring rapidly. Diminished blood flow in hydronephrosis has been well-documented by others, and therefore our results are consistent with studies which have shown mild ischemia to be the cause of tissue atrophy involving apoptosis. We conclude that cell deletion by apoptosis plays an important role in the pathogenesis of renal tubular atrophy associated with hydronephrosis.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
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Created: Wed, 09 Mar 2011, 08:32:08 EST