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Imatinib suppresses cryoglobulinemia and secondary membranoproliferative glomerulonephritis #MMPMID19020005
Iyoda M; Hudkins KL; Becker-Herman S; Wietecha TA; Banas MC; Guo S; Meyer-Bahlburg A; Kowalewska J; Liu G; Ziegler SF; Rawlings DJ; Alpers CE
J Am Soc Nephrol 2009[Jan]; 20 (1): 68-77 PMID19020005show ga
Imatinib is a receptor tyrosine kinase inhibitor that blocks the activity of c-Abl, c-Kit, and PDGF receptors. We tested the protective effects of imatinib in thymic stromal lymphopoietin transgenic mice, a model of cryoglobulinemia and associated membranoproliferative glomerulonephritis (MPGN), in which some glomerular manifestations likely result from PDGF receptor activation. Surprising, administration of imatinib beginning at weaning suppressed production of cryoglobulin, attenuating both the renal injury and systemic features of cryoglobulinemia. Flow cytometry suggested that inhibition of B cell development in the bone marrow likely caused the reduction in cryoglobulin production. In addition, administration of imatinib to thymic stromal lymphopoietin transgenic mice with established MPGN also diminished cryoglobulin production and reversed the renal and systemic lesions. These data suggest that treatment with imatinib may be a novel therapeutic approach for cryoglobulinemia and MPGN in humans.
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J+Am+Soc+Nephrol 2009 ; 20 (1): 68-77
