Mycophenolate mofetil in ongoing chronic kidney allograft dysfunction

Senn, Beatrice M.; Rochat, Ph; Schwarzkopf, Andreas; Weinreich, T; Binswanger, U

doi:10.1016/s0041-1345(98)01346-3

Cited by 2 publications

(1 citation statement)

References 2 publications

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“…So, if rapamycin is to be used in conjunction with a calcineurin inhibitor, the dose of the calcineurin inhibitor should be reduced accordingly and careful attention paid to whole blood drug levels. Despite its ef®cacy in inhibiting acute rejection and proliferation 138,154,155 , rapamycin's role in the prevention of allograft ®brosis may be counteracted by its hypercholesterolaemic and hyperlipidaemic effects 143 . Clinical trials on rapamycin are under way, although so far none is assessing the impact of rapamycin on CGN.…”

Section: Immunosuppressive Drugsmentioning

confidence: 99%

Molecular mechanisms of renal allograft fibrosis

Waller

Nicholson

2001

Journal of British Surgery

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Recent advances in understanding of the underlying molecular mechanisms involved suggest autocrine secretion of cytokines and growth factors, especially transforming growth factor beta, are associated with a change in fibroblast phenotype leading to the deposition of extracellular matrix. Repeated insults trigger upregulation of the tissue inhibitors of matrix metalloproteinases, favouring accumulation of extracellular matrix. To date, no drug has proved effective in inhibiting or reducing allograft fibrosis. The deleterious consequences of chronic immunosuppression on the development of such fibrosis are now recognized; newer immunosuppressive drugs, including rapamycin and mycophenolate mofetil, reduce profibrotic gene expression in both experimental and clinical settings, and offer potential strategies for prolonging allograft survival.

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Section: Immunosuppressive Drugsmentioning

confidence: 99%