Abstract
The use of cyclosporin A (CsA) in both organ transplantation and in the treatment of autoimmune disease may ultimately be limited by the drug’s nephrotoxic properties (Klintmalm et al, 1981). Indeed a major clinical problem has been the differentiation of rejection from CsA-induced nephrotoxicity, following renal transplantation. This nephrotoxicity is characterised by impaired renal function and histologically, predominantly by tubular changes (Blair et al, 1982; Thiru et al, 1983). Although the pathogenesis of CsA-induced nephrotoxicity is still unclear, alterations in glomerulotubular function have been demonstrated (Battle et al, 1986; Gnutzman et al, 1986; Dieperink et al, 1986a, b).
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© 1989 Springer Science+Business Media New York
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Whiting, P.H., Propper, D.J., Simpson, J.G., McKay, J., Jones, M.C., Catto, G.R.D. (1989). Renal Tubular Function in Experimental and Clinical Cyclosporin (CsA) Nephrotoxicity. In: Bach, P.H., Lock, E.A. (eds) Nephrotoxicity. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-2040-2_43
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DOI: https://doi.org/10.1007/978-1-4757-2040-2_43
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