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10.2169/internalmedicine.56.7778 http://scihub22266oqcxt.onion/10.2169/internalmedicine.56.7778 28381748!5457925!28381748     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28381748&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Intern+Med 2017 ; 56 (7): 811-817 Nephropedia Template TP {{tp|p=28381748|t=2017. Post-infectious Proliferative Glomerulonephritis with Monoclonal Immunoglobulin G Deposits Associated with Complement Factor H Mutation |pdf=|usr=}}{{28381748}} gab.com Text Post-infectious Proliferative Glomerulonephritis with Monoclonal Immunoglobulin G Deposits Associated with Complement Factor H Mutation JO: Intern Med http://www.kidney.de/pget.php?&tw=1&pmid=28381748 #FOAvip A 55-year-old man developed rapidly progressive glomerulonephritis and nephrotic syndrome. A kidney biopsy specimen showed diffuse proliferative and crescentic glomerulonephritis with monoclonal IgG1kappa, humps, and nephritis-associated plasmin receptor, indicating infection-associated proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID). Despite dialysis-dependent renal failure, symptomatic therapy resulted in spontaneous recovery of the renal function, mimicking post-infectious glomerulonephritis (PIGN). A heterozygous complement factor H mutation was detected by comprehensive genetic testing of alternative pathway regulatory genes, which might lead to persistent infection-triggered alternative pathway activation and account for severe glomerulonephritis. Post-infectious PGNMID and PIGN might share common clinical presentations and pathogenesis related to the complement pathway. Twit Text FOAVip Post-infectious Proliferative Glomerulonephritis with Monoclonal Immunoglobulin G Deposits Associated with Complement Factor H Mutation ????Intern Med http://www.kidney.de/pget.php?&tw=1&pmid=28381748 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28381748 #FOAvip English Wikipedia <ref>{{Cite pmid|28381748}}</ref> Post-infectious Proliferative Glomerulonephritis with Monoclonal Immunoglobulin G Deposits Associated with Complement Factor H Mutation #MMPMID28381748 Takehara E; Mandai S; Shikuma S; Akita W; Chiga M; Mori T; Oda T; Kuwahara M; Uchida S Intern Med 2017[]; 56 (7): 811-817 PMID28381748show ga A 55-year-old man developed rapidly progressive glomerulonephritis and nephrotic syndrome. A kidney biopsy specimen showed diffuse proliferative and crescentic glomerulonephritis with monoclonal IgG1kappa, humps, and nephritis-associated plasmin receptor, indicating infection-associated proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID). Despite dialysis-dependent renal failure, symptomatic therapy resulted in spontaneous recovery of the renal function, mimicking post-infectious glomerulonephritis (PIGN). A heterozygous complement factor H mutation was detected by comprehensive genetic testing of alternative pathway regulatory genes, which might lead to persistent infection-triggered alternative pathway activation and account for severe glomerulonephritis. Post-infectious PGNMID and PIGN might share common clinical presentations and pathogenesis related to the complement pathway. |Complement Factor H/genetics[MESH] |Glomerulonephritis, Membranoproliferative/drug therapy/*physiopathology[MESH] |Humans[MESH] |Immunoglobulin G/*metabolism[MESH] |Male[MESH] |Middle Aged[MESH] |Mutation[MESH] |Receptors, Peptide/metabolism[MESH] |Renal Dialysis[MESH]Post-infectious Proliferative Glomerulonephritis with Monoclonal Immun(epmc).pdf DeepDyve Pubget Overpricing