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10.1007/s13730-014-0135-0 http://scihub22266oqcxt.onion/10.1007/s13730-014-0135-0 C5413710!5413710!28509266     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       CEN+Case+Rep 2015 ; 4 (1): 31-7 Nephropedia Template TP {{tp|p=28509266|t=2015. A case of gefitinib-associated membranous nephropathy in treatment for pulmonary adenocarcinoma |pdf=|usr=}}{{28509266}} gab.com Text A case of gefitinib-associated membranous nephropathy in treatment for pulmonary adenocarcinoma JO: CEN Case Rep http://www.kidney.de/pget.php?&tw=1&pmid=28509266 #FOAvip We experienced a case that was considered as gefitinib-associated membranous nephropathy (MGN) in treatment for pulmonary adenocarcinoma. A female patient aged 80 who had been treated for lung cancer was referred and hospitalized at our hospital, because of nephrotic syndrome. The patient had pulmonary adenocarcinoma (cT4N2M1a) with positive for epidermal growth factor receptor (EGFR) mutation. Gefitinib, EGFR tyrosine kinase inhibitor, was initiated from 1 year and 2 months ago. At that time, proteinuria was negative. The treatment effect on lung cancer was so favorable that partial response had been maintained. However, from 4 months ago, edema of legs appeared, leading to become nephrotic syndrome. Renal biopsy was performed, and secondary MGN was diagnosed, because of deposition of peripheral IgG, mesangial IgA, and C3, as well as the deposition of peripheral IgG4, IgG1, IgG2, and weak IgG3. We considered drug-induced MGN and discontinued the administration of gefitinib. Subsequently, the proteinuria tended to decrease gradually and became negative 10 months later. However, the lung cancer recurred 3 months after discontinuation of gefitinib and another molecular target drug, erlotinib, was administered. At present, 13 months after discontinuation of gefitinib, absence of proteinuria is maintained. It has been generally considered that secondary MGN can be induced by both malignant tumor and their treatment. In the present case, the clinical course and pathological characteristics showed the secondary MGN that might be associated with gefitinib during the treatment for pulmonary adenocarcinoma. The present case, to our knowledge, may be a first case of gefitinib-associated MGN. Twit Text FOAVip A case of gefitinib-associated membranous nephropathy in treatment for pulmonary adenocarcinoma ????CEN Case Rep http://www.kidney.de/pget.php?&tw=1&pmid=28509266 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28509266 #FOAvip English Wikipedia <ref>{{Cite pmid|28509266}}</ref> A case of gefitinib-associated membranous nephropathy in treatment for pulmonary adenocarcinoma #MMPMID28509266 Kaneko T; Shimizu A; Aoki M; Tsuruoka S CEN Case Rep 2015[May]; 4 (1): 31-7 PMID28509266show ga We experienced a case that was considered as gefitinib-associated membranous nephropathy (MGN) in treatment for pulmonary adenocarcinoma. A female patient aged 80 who had been treated for lung cancer was referred and hospitalized at our hospital, because of nephrotic syndrome. The patient had pulmonary adenocarcinoma (cT4N2M1a) with positive for epidermal growth factor receptor (EGFR) mutation. Gefitinib, EGFR tyrosine kinase inhibitor, was initiated from 1 year and 2 months ago. At that time, proteinuria was negative. The treatment effect on lung cancer was so favorable that partial response had been maintained. However, from 4 months ago, edema of legs appeared, leading to become nephrotic syndrome. Renal biopsy was performed, and secondary MGN was diagnosed, because of deposition of peripheral IgG, mesangial IgA, and C3, as well as the deposition of peripheral IgG4, IgG1, IgG2, and weak IgG3. We considered drug-induced MGN and discontinued the administration of gefitinib. Subsequently, the proteinuria tended to decrease gradually and became negative 10 months later. However, the lung cancer recurred 3 months after discontinuation of gefitinib and another molecular target drug, erlotinib, was administered. At present, 13 months after discontinuation of gefitinib, absence of proteinuria is maintained. It has been generally considered that secondary MGN can be induced by both malignant tumor and their treatment. In the present case, the clinical course and pathological characteristics showed the secondary MGN that might be associated with gefitinib during the treatment for pulmonary adenocarcinoma. The present case, to our knowledge, may be a first case of gefitinib-associated MGN. äA case of gefitinib-associated membranous nephropathy in treatment for(epmc).pdf DeepDyve Pubget Overpricing