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10.1007/s13730-013-0060-7 http://scihub22266oqcxt.onion/10.1007/s13730-013-0060-7 C5411549!5411549 !28509295     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28509295 &cmd=llinks): Failed to open stream: HTTP request failed! 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Antineutrophil cytoplasmic antibody-associated crescentic glomerulonephritis with membranous nephropathy treated using thiamazole |pdf=|usr=}}{{28509295 }} gab.com Text Antineutrophil cytoplasmic antibody-associated crescentic glomerulonephritis with membranous nephropathy treated using thiamazole JO: CEN Case Rep http://www.kidney.de/pget.php?&tw=1&pmid=28509295 #FOAvip A 21-year-old woman with nephrotic syndrome was referred to our hospital. She had congenital diaphragmatic hernia, hypoxic ischemic encephalopathy, and mental retardation, and had been treated for hyperthyroidism with thiamazole in another hospital. Serum creatinine was 37.8 ?mol/L and antineutrophil cytoplasmic antibody against myeloperoxidase (MPO-ANCA) was 39 EU. Urinalyses were 3+ for proteins and 3+ for occult blood. A renal biopsy was performed. An examination using light microscopy (LM) revealed necrotizing glomerulonephritis with crescent formation. Immunofluorescence microscopy showed granular staining with immunoglobulin G and complement component 3 along the capillary walls. Electron microscopy (EM) disclosed subepithelial dense deposits. A renal biopsy suggested necrotizing glomerulonephritis with membranous nephropathy (MN) in stages I or II. Since many cases of drug-induced ANCA-associated glomerulonephritis (AAG) have been reported, we stopped thiamazole and treated with corticosteroid. The MPO-ANCA titer became negative 49 days after the initiation of treatment. Two years after the first treatment, the MPO-ANCA titer became elevated again and was 82 EU. The patient was administered cyclophosphamide and prednisone. However, the MPO-ANCA titer did not decrease. A renal biopsy was performed again 3 years after the first renal biopsy. LM revealed no crescentic formation but demonstrated spike formations along the glomerular basement membrane. EM also disclosed subepithelial dense deposits, but less than the first biopsy. The renal biopsy suggested MN in stages II or III. AAG was regarded as inactive after corticosteroid treatment. Therefore, ciclosporin administration was started. In conclusion, we experienced a rare case of AAG complicated with MN. The histopathologic results showed that immunosuppressive therapy seemed to be effective in treating crescentic glomerulonephritis; furthermore, it reduced proteinuria but could not reduce the MPO-ANCA titer. Twit Text FOAVip Antineutrophil cytoplasmic antibody-associated crescentic glomerulonephritis with membranous nephropathy treated using thiamazole ????CEN Case Rep http://www.kidney.de/pget.php?&tw=1&pmid=28509295 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28509295 #FOAvip English Wikipedia <ref>{{Cite pmid|28509295 }}</ref> Antineutrophil cytoplasmic antibody-associated crescentic glomerulonephritis with membranous nephropathy treated using thiamazole #MMPMID28509295 Kakita T ; Nagatoya K ; Takimoto H ; Matsuda H ; Mori T ; Kawaguchi A ; Inoue T CEN Case Rep 2013[Nov]; 2 (2 ): 165-169 PMID28509295 show ga A 21-year-old woman with nephrotic syndrome was referred to our hospital. She had congenital diaphragmatic hernia, hypoxic ischemic encephalopathy, and mental retardation, and had been treated for hyperthyroidism with thiamazole in another hospital. Serum creatinine was 37.8 ?mol/L and antineutrophil cytoplasmic antibody against myeloperoxidase (MPO-ANCA) was 39 EU. Urinalyses were 3+ for proteins and 3+ for occult blood. A renal biopsy was performed. An examination using light microscopy (LM) revealed necrotizing glomerulonephritis with crescent formation. Immunofluorescence microscopy showed granular staining with immunoglobulin G and complement component 3 along the capillary walls. Electron microscopy (EM) disclosed subepithelial dense deposits. A renal biopsy suggested necrotizing glomerulonephritis with membranous nephropathy (MN) in stages I or II. Since many cases of drug-induced ANCA-associated glomerulonephritis (AAG) have been reported, we stopped thiamazole and treated with corticosteroid. The MPO-ANCA titer became negative 49 days after the initiation of treatment. Two years after the first treatment, the MPO-ANCA titer became elevated again and was 82 EU. The patient was administered cyclophosphamide and prednisone. However, the MPO-ANCA titer did not decrease. A renal biopsy was performed again 3 years after the first renal biopsy. LM revealed no crescentic formation but demonstrated spike formations along the glomerular basement membrane. EM also disclosed subepithelial dense deposits, but less than the first biopsy. The renal biopsy suggested MN in stages II or III. AAG was regarded as inactive after corticosteroid treatment. Therefore, ciclosporin administration was started. In conclusion, we experienced a rare case of AAG complicated with MN. The histopathologic results showed that immunosuppressive therapy seemed to be effective in treating crescentic glomerulonephritis; furthermore, it reduced proteinuria but could not reduce the MPO-ANCA titer. äAntineutrophil cytoplasmic antibody-associated crescentic glomerulonep(epmc).pdf DeepDyve Pubget Overpricing