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10.1097/MD.0000000000007144 http://scihub22266oqcxt.onion/10.1097/MD.0000000000007144 C5478328!5478328 !28614243     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28614243 &cmd=llinks): Failed to open stream: HTTP request failed! 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Different types of glomerulonephritis associated with the dysregulation of the complement alternative pathway in 2 brothers: A case report |pdf=|usr=}}{{28614243 }} gab.com Text Different types of glomerulonephritis associated with the dysregulation of the complement alternative pathway in 2 brothers: A case report JO: Medicine (Baltimore) http://www.kidney.de/pget.php?&tw=1&pmid=28614243 #FOAvip RATIONALE: C3 glomerulonephritis (C3GN) and complement-mediated hemolytic uremic syndrome (HUS) both result from the abnormal regulation of the complement system. A significant number of patients with C3GN or complement-mediated HUS have mutations of more than 1 complement protein. This discovery has had a major impact on identifying the underlying cause of familial C3GN or complement-mediated HUS. PATIENT CONCERNS: We report the cases of 2 brothers (herein referred to as patient II-1 and patient II-9), both with complement disorders that differed in their clinical and genetic features. DIAGNOSES: Patient II-1 clinically presented with nephrotic syndrome and acute kidney injury and pathologically presented with C3GN combined with thrombotic microangiopathy (TMA) and subacute tubulointerstitial nephritis. Meanwhile, patient II-9 clinically presented with HUS and pathologically presented with TMA combined with acute severe tubular injury. INTERVENTIONS: Screenings for genetic mutations contributed to complement system dysregulation were performed on patient II-1. OUTCOMES: The genome sequencing identified that patient II-1 had a heterozygous mutation in the C3 gene (c.C1774T/p.R592W). Nine other relatives of the brothers were checked for this C3 mutation and only the daughter of patient II-1 (herein referred to as patient III-2) carried it, but so far, she does not have any clinical manifestations of kidney disease. LESSIONS: Family members with a dysregulation of the complement alternative pathway may differ in its clinical and genetic features. Twit Text FOAVip Different types of glomerulonephritis associated with the dysregulation of the complement alternative pathway in 2 brothers: A case report ????Medicine (Baltimore) http://www.kidney.de/pget.php?&tw=1&pmid=28614243 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28614243 #FOAvip English Wikipedia <ref>{{Cite pmid|28614243 }}</ref> Different types of glomerulonephritis associated with the dysregulation of the complement alternative pathway in 2 brothers: A case report #MMPMID28614243 Chen P ; Zhu L ; Yu F ; Han SS ; Meng SJ ; Guo WY ; Zhang H ; Song Y Medicine (Baltimore) 2017[Jun]; 96 (24 ): e7144 PMID28614243 show ga RATIONALE: C3 glomerulonephritis (C3GN) and complement-mediated hemolytic uremic syndrome (HUS) both result from the abnormal regulation of the complement system. A significant number of patients with C3GN or complement-mediated HUS have mutations of more than 1 complement protein. This discovery has had a major impact on identifying the underlying cause of familial C3GN or complement-mediated HUS. PATIENT CONCERNS: We report the cases of 2 brothers (herein referred to as patient II-1 and patient II-9), both with complement disorders that differed in their clinical and genetic features. DIAGNOSES: Patient II-1 clinically presented with nephrotic syndrome and acute kidney injury and pathologically presented with C3GN combined with thrombotic microangiopathy (TMA) and subacute tubulointerstitial nephritis. Meanwhile, patient II-9 clinically presented with HUS and pathologically presented with TMA combined with acute severe tubular injury. INTERVENTIONS: Screenings for genetic mutations contributed to complement system dysregulation were performed on patient II-1. OUTCOMES: The genome sequencing identified that patient II-1 had a heterozygous mutation in the C3 gene (c.C1774T/p.R592W). Nine other relatives of the brothers were checked for this C3 mutation and only the daughter of patient II-1 (herein referred to as patient III-2) carried it, but so far, she does not have any clinical manifestations of kidney disease. LESSIONS: Family members with a dysregulation of the complement alternative pathway may differ in its clinical and genetic features. |*Complement Pathway, Alternative [MESH] |Adult [MESH] |Complement System Proteins/*genetics/*metabolism [MESH] |Fatal Outcome [MESH] |Glomerulonephritis/*genetics/*metabolism/pathology/therapy [MESH] |Humans [MESH] |Male [MESH] |Middle Aged [MESH] |Mutation [MESH]Different types of glomerulonephritis associated with the dysregulatio(epmc).pdf DeepDyve Pubget Overpricing