Peritubular capillary injury during the progression of experimental glomerulonephritis in rats

The functional and morphologic changes occurring in the peritubular capillaries (PTC) of the kidney during the progression of renal disease are not yet completely understood. In this study, the features of PTC disruption observed in a rat anti-glomerular basement membrane-induced glomerulonephritis...

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Bibliographic Details
Published in:Journal of the American Society of Nephrology 2000, Vol.11 (1), p.47-56
Main Authors: OHASHI, R, KITAMURA, H, YAMANAKA, N
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Capillaries - pathology
Cell Death
Disease Models, Animal
Disease Progression
Glomerulonephritis
Glomerulonephritis - pathology
Glomerulonephritis - physiopathology
Kidney Function Tests
Kidney Tubules - blood supply
Kidney Tubules - injuries
Male
Medical sciences
Nephrology. Urinary tract diseases
Nephropathies. Renovascular diseases. Renal failure
Rats
Rats, Inbred WKY
Statistics, Nonparametric
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Summary:The functional and morphologic changes occurring in the peritubular capillaries (PTC) of the kidney during the progression of renal disease are not yet completely understood. In this study, the features of PTC disruption observed in a rat anti-glomerular basement membrane-induced glomerulonephritis (GN) model were characterized. Contributions to the progression of the disease made by other interstitial components, including ED-1-positive macrophages and CD3-positive T cells, were also investigated. Within 7 d of inducing GN, severe necrotizing glomerular injuries were observed. Thrombomodulin staining revealed that within 3 to 8 wk, there was a significant (P < 0.001) decline in the number of PTC, accompanied by a marked accumulation of macrophages, T cells, and fibrotic material. By the end of this period, most PTC were severely damaged or lost, and tubulointerstitial scarring was noted in the affected areas. Furthermore, PTC endothelial cell apoptosis occurred concomitantly, as shown by application of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling methods and electron microscopy. It was presumed that the PTC injury was mediated possibly by the infiltrating macrophages and T cells, which, together with destruction of the PTC structure, correlated significantly with the impairment of renal function. These findings suggest that PTC disruption and the subsequent regression of the capillary network may contribute to the development of the tubulointerstitial injury largely responsible for the renal dysfunction in progressive GN.
ISSN:1046-6673
1533-3450
DOI:10.1681/asn.v11147