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Journal of the Korean Society of Pediatric Nephrology 2002;6(2): 142-154.
미세변화 신증후군 환아에서 사이클로스포린 치료 후 Osteopontin과 Transforming Growth Factor-${beta}$의 발현
임범진, 김병길, 홍순원, 정현주
1연세대학교 의과대학 병리학교실
2연세대학교 의과대학 소아과학교실
3연세대학교 의과대학 병리학교실
4연세대학교 의과대학 병리학교실
Expression of Osteopontin and Transforming Growth Factor- ${beta}$ in Childhood Minimal Change Nephrotic Syndrome After Cyclosporine Treatment
Beom-Jin Lim, Pyung-Kil Kim, Soon-Won Hong, Hyeon-Joo Jeong
1Dept. of Pathology, Yonsei University, College of Medicine
2Dept. of Pediatrics, Yonsei University, College of Medicine
3Dept. of Pathology, Yonsei University, College of Medicine
4Dept. of Pathology, Yonsei University, College of Medicine
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ABSTRACT
Purpose : One of the most important adverse effects of long-term cyclosporine therapy is nephrotoxicity, the morphologic changes of which include interstitial fibrosis and arteriolar hyalinization. Recently, several authors have shown that osteopontin plays an important role in the development of interstitial fibrosis by acting as a macrophage chemoattractant and stimulating the production of $TGF-{beta}$ in experimental cyclosporine nephrotoxicity. However, the relationship between osteopontin and $TGF-{beta}$ in humans has not been clearly documented so far. We studied the expression of osteopontin and $TGF-{beta}$ in children with minimal change nephrotic syndrome treated with cyclosporine to demonstrate whether there is a relationship between cyclosporine toxicity and osteopontin expression as previously shown in animal models.
Materials and methods : Nineteen children (15 males and 4 females) were the subject of this study. Renal biopsies had been performed before and after the cyclosporine therapy (mean duration: 15.9 months). In 5 patients, additional biopsies were performed after completing the cyclosporine treatment (mean; 26 months). The expressions of osteopontin and $TGF-{beta}$ were evaluated by immunohistochemistry in the glomeruli and tubulointerstitium.
Results : Osteopontin expression was significantly increased in the glomerular mesangium and tubules after cyclosporine treatment. But there was no statistically significant increase of $TGF-{beta}$ in the interstitium. There was no significant increase in tubular osteopontin and interstitial $TGF-{beta}$ expression in those cases developing interstitial fibrosis after cyclosporine treatment compared with cases those not developing interstitial fibrosis. No significant changes in osteopontin or $TGF-{beta}$ expression were observed in subsequent 5 biopsy samples after discontinuation of cyclosporine compared with the first follow up biopsies.
Conclusion : These results suggest that osteopontin is a nonspecific marker of renal injury rather than a mediator of interstitial fibrosis in cyclosporine nephrotoxicity of human.
Key words: Cyclosporine | Nephrotoxicity | Human | Biopsy
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