Comparison between Osteopontin Expression and Renal Function in Spontaneous Renal Failure Model.
- Author:
Duk Hyun LEE
1
;
Sang Ki KIM
;
Joong Ha HWANG
;
Byoung Hwa HYUN
;
Yong Jin KIM
Author Information
1. Department of Internal Medicine, Fatima Hospital, Daegu, Korea.
- Publication Type:Original Article
- Keywords:
Tubulointerstitial injury;
Osteopontin;
Monocyte/macrophages
- MeSH:
Adhesives;
Animals;
Atrophy;
Collagen;
Fibrosis;
Glomerulonephritis;
Glycoproteins;
Inflammation;
Mice;
Models, Theoretical;
Osteopontin*;
Proteinuria;
Renal Insufficiency*
- From:Korean Journal of Nephrology
2000;19(5):819-826
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Tubuolointerstitial inflammation and tubular injury account for most types of glomerulonephritis. The injury is characterized by an infiltration of mononuclear cells with atrophy and dilation of tubules and increased deposition of collagen in the interstitium. Despite the fact that the degree of tubulointerstitial injury in glomerular diseases may be the best predictor of overall outcome, the pathogenic mechanism by which the tubular injury develops remains unknown. Osteopontin, a highly acidic, phosphorylated, secreted glycoprotein, is up-regulated in renal cortex in many experimental models of tubulointerstitial fibrosis. In this study, we examined the expression of osteopontin in tubulointerstitium in experimental renal failure mouse, FGS/KIST. Mice were assigned three groups and sacrificed at 1 month, 2 months, and 3 months, in each. Proteinuria, GFR, the degree of tubulointerstitial inflammation, tubular atrophy, glomerulosclerosis and osteopontin expression were measured. Three-month-old group showed severely decreased GFR and marked tubulointerstitial inflammation and glomerulosclerosis compared with other groups. The expression of osteopontin increased with the severity of tubulointerstitial injury. These data suggest that osteopontin may act as a chemotactic or adhesive factor in the recruitment of the monocyte/macrophages and have a role in the pathogenesis of the tubulointerstitial injury.
