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10.1053/j.ackd.2014.06.001 http://scihub22266oqcxt.onion/10.1053/j.ackd.2014.06.001 C4197186!4197186 !25168831     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25168831 &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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25168831 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Adv+Chronic+Kidney+Dis 2014 ; 21 (5 ): 422-5 Nephropedia Template TP {{tp|p=25168831 |t=2014. Familial FSGS |pdf=|usr=}}{{25168831 }} gab.com Text Familial FSGS JO: Adv Chronic Kidney Dis http://www.kidney.de/pget.php?&tw=1&pmid=25168831 #FOAvip Focal segmental glomerulosclerosis (FSGS) and nephrotic syndrome can be caused by rare highly penetrant mutations in number of genes. FSGS can follow both recessive and dominant inheritance patterns. In general, recessive forms present early, whereas the autosomal dominant forms present in adolescence or adulthood. Many of the genes found to be mutated in FSGS and nephrotic syndrome patients encode proteins essential for normal podocyte structure and/or function. An exception appears to be APOL1, which harbors common variants responsible for the high rate of FSGS and other nephropathies in people of recent African ancestry. Familial FSGS should be regarded as part of a spectrum of inherited glomerulopathies where the precise histologic presentation may depend on the age of onset, function of the responsible gene and gene products, and other factors. Twit Text FOAVip Familial FSGS ????Adv Chronic Kidney Dis http://www.kidney.de/pget.php?&tw=1&pmid=25168831 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25168831 #FOAvip English Wikipedia <ref>{{Cite pmid|25168831 }}</ref> Familial FSGS #MMPMID25168831 Pollak MR Adv Chronic Kidney Dis 2014[Sep]; 21 (5 ): 422-5 PMID25168831 show ga Focal segmental glomerulosclerosis (FSGS) and nephrotic syndrome can be caused by rare highly penetrant mutations in number of genes. FSGS can follow both recessive and dominant inheritance patterns. In general, recessive forms present early, whereas the autosomal dominant forms present in adolescence or adulthood. Many of the genes found to be mutated in FSGS and nephrotic syndrome patients encode proteins essential for normal podocyte structure and/or function. An exception appears to be APOL1, which harbors common variants responsible for the high rate of FSGS and other nephropathies in people of recent African ancestry. Familial FSGS should be regarded as part of a spectrum of inherited glomerulopathies where the precise histologic presentation may depend on the age of onset, function of the responsible gene and gene products, and other factors. |*Mutation [MESH] |Apolipoprotein L1 [MESH] |Apolipoproteins/genetics [MESH] |Black People/genetics [MESH] |Genetic Predisposition to Disease [MESH] |Glomerulosclerosis, Focal Segmental/*genetics [MESH] |Humans [MESH]Familial FSGS (epmc).pdf DeepDyve Pubget Overpricing