The DOI matches its Crossref record; 22 of the 22 references it cites were found in a registry or an index.
Pathogenesis of cyclosporine nephropathy: roles of angiotensin II and osteopontin.
Abstract
Low-salt-diet, cyclosporine (CsA; 15 mg/kg per day)-treated rats develop striped interstitial fibrosis, arteriolar hyalinosis, and azotemia similar to the chronic nephropathy observed in humans. To examine the role of angiotensin II in this model, rats on a low-salt diet were given CsA, CsA and the angiotensin II receptor Type I antagonist Losartan (10 mg/kg per day), CsA and hydralazine/furosemide, or vehicle. At Day 35, CsA-treated rats had tubular injury, arteriolopathy of the afferent arteriole, increased expression of the monocyte-macrophage adhesive protein osteopontin, interstitial macrophage infiltration, increased interstitial transforming growth factor-beta expression, and interstitial fibrosis. This study provides new insight in both pathogenic and therapeutic aspects of CsA nephropathy. The pathogenesis of CsA nephropathy involves the expression of osteopontin by tubular epithelial cells, the level of which closely correlates with the degree of macrophage infiltration and interstitial fibrosis in all groups (r = 0.79 and 0.74, respectively; P < 0.001). Therapeutic conclusions can be drawn from the observation that both losartan and hydralazine/furosemide reduced osteopontin expression, macrophage infiltration, transforming growth factor-beta expression, and interstitial fibrosis, but did not prevent the decrease in GFR. Treatment with losartan, but not with hydralazine and furosemide, markedly reduced arteriolopathy. It was concluded that angiotensin II contributes to the vasculopathy (hyalinosis) induced by CsA. In contrast, the interstitial fibrosis mediated by CsA can be partially prevented by both an angiotensin II Type I receptor antagonist or by hydralazine and furosemide. This suggests that the interstitial fibrosis can be dissociated from the vascular effects of CsA. The beneficial effects of lowering blood pressure or vasodilation per se may be difficult to distinguish from the specific effects of angiotensin II receptor blockade.
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Citations
Cites
CYCLOSPORIN A IN PATIENTS RECEIVING RENAL ALLOGRAFTS FROM CADAVER DONORS
Calne, R. Y., Thiru, S., Mcmaster, P., Craddock, G. N., White, D. J. G., Evans, D. B., Dunn, D. C., Pentlow, B. D., & Rolles, K. (1978) · The Lancet · doi:10.1016/s0140-6736(78)91970-0 · Cited by 1,002
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Self-citationRenal injury from angiotensin II-mediated hypertension.
Johnson, R. J., Alpers, C. E., Yoshimura, A., Lombardi, D., Pritzl, P., Floege, J., & Schwartz, S. M. (1992) · Hypertension · doi:10.1161/01.hyp.19.5.464 · Cited by 536
Self-citationInflammatory and immunomodulatory roles of TGF-β
Wahl, S. M., McCartney-Francis, N., & Mergenhagen, S. E. (1989) · Immunology Today · doi:10.1016/0167-5699(89)90136-9 · Cited by 449
Effect of cyclosporine administration on renal hemodynamics in conscious rats
Murray, B. M., Paller, M. S., & Ferris, T. F. (1985) · Kidney International · doi:10.1038/ki.1985.196 · Cited by 419
Sustained expression of TGF-β1 underlies development of progressive kidney fibrosis
Yamamoto, T., Noble, N. A., Miller, D. E., & Border, W. A. (1994) · Kidney International · doi:10.1038/ki.1994.122 · Cited by 405
Floege, J., Burns, M. W., Alpers, C. E., Yoshimura, A., Pritzl, P., Gordon, K., Seifert, R. A., Bowen-Pope, D. F., Couser, W. G., & Johnson, R. J. (1992) · Kidney International · doi:10.1038/ki.1992.42 · Cited by 404
Self-citationShiraga, H., Min, W., VanDusen, W. J., Clayman, M. D., Miner, D., Terrell, C. H., Sherbotie, J. R., Foreman, J. W., Przysiecki, C., & Neilson, E. G. (1992) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.89.1.426 · Cited by 390
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Patarca, R., Freeman, G. J., Singh, R. P., Wei, F. Y., Durfee, T., Blattner, F., Regnier, D. C., Kozak, C. A., Mock, B. A., & Morse, H. C. (1989) · The Journal of experimental medicine · doi:10.1084/jem.170.1.145 · Cited by 322
Cited by
Role of the Microvascular Endothelium in Progressive Renal Disease
Kang, D.-H., Kanellis, J., Hugo, C., Truong, L., Anderson, S., Kerjaschki, D., Schreiner, G. F., & Johnson, R. J. (2002) · Journal of the American Society of Nephrology · doi:10.1681/asn.v133806 · Cited by 466
Self-citationSubtle Acquired Renal Injury as a Mechanism of Salt-Sensitive Hypertension
Johnson, R. J., Herrera-Acosta, J., Schreiner, G. F., & Rodríguez-Iturbe, B. (2002) · New England Journal of Medicine · doi:10.1056/nejmra011078 · Cited by 448
The role of osteopontin in foreign body giant cell formation
Tsai, A. T., Rice, J., Scatena, M., Liaw, L., Ratner, B. D., & Giachelli, C. M. (2005) · Biomaterials · doi:10.1016/j.biomaterials.2005.03.003 · Cited by 71
Metadata
- Authors
- Pichler, R. H., Franceschini, N., Young, B. A., Hugo, C., Andoh, T. F., Burdmann, E. A., Shankland, S. J., Alpers, C. E., Bennett, W. M., & Couser, W. G.
- Venue
- Journal of the American Society of Nephrology
- Published
- 1995-10
- Volume
- 6
- Issue
- 4
- Pages
- 1186-1196
- ISSN
- 1046-6673 (ISSN-L)
- OpenAlex
- W2098945680
- Cited by
- 256
- References
- 22
- FWCI
- 10.30
- Type
- journal article
- Language
- en
- Open access
- closed
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- Pichler, R. H., Franceschini, N., Young, B. A., Hugo, C., Andoh, T. F., Burdmann, E. A., Shankland, S. J., Alpers, C. E., Bennett, W. M., & Couser, W. G. (1995). Pathogenesis of cyclosporine nephropathy: roles of angiotensin II and osteopontin. Journal of the American Society of Nephrology. https://doi.org/10.1681/asn.v641186
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