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10.1053/j.ajkd.2016.01.030 http://scihub22266oqcxt.onion/10.1053/j.ajkd.2016.01.030 C4921260!4921260!27085376     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Kidney+Dis 2016 ; 68 (1): 138-47 Nephropedia Template TP {{tp|p=27085376|t=2016. Membranous Nephropathy: A Journey From Bench to Bedside |pdf=|usr=}}{{27085376}} gab.com Text Membranous Nephropathy: A Journey From Bench to Bedside JO: Am J Kidney Dis http://www.kidney.de/pget.php?&tw=1&pmid=27085376 #FOAvip Lessons from an animal model that faithfully resembles human membranous nephropathy (MN) have informed our understanding of the pathogenesis of this organ-specific autoimmune disease and common cause of the nephrotic syndrome. Once it was established that the subepithelial immune deposits that characterize experimental MN form in situ when circulating antibodies bind to an intrinsic podocyte antigen, it was merely a matter of time before the human antigen was identified. The M-type phospholipase A2 receptor 1 (PLA2R) represents the major target antigen in primary MN, and thrombospondin type 1 domain-containing 7A (THSD7A) was more recently identified as a minor antigen. Serological tests for anti-PLA2R as well as kidney biopsy specimen staining for PLA2R exhibit more than 90% specificity and 70% to 80% sensitivity for the diagnosis of primary MN in most populations. The assays distinguish most cases of primary MN from MN associated with other systemic diseases, and sequential titers of anti-PLA2R are useful to monitor treatment response. A positive pre-transplantation test for anti-PLA2R is also helpful for predicting the risk of post-transplantation recurrence. Identification of target epitopes within PLA2R as well as the genetic association of primary MN with class II major histocompatibility and PLA2R1 variants are 2 additional examples of our evolving understanding of this disease. Twit Text FOAVip Membranous Nephropathy: A Journey From Bench to Bedside ????Am J Kidney Dis http://www.kidney.de/pget.php?&tw=1&pmid=27085376 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27085376 #FOAvip English Wikipedia <ref>{{Cite pmid|27085376}}</ref> Membranous Nephropathy: A Journey From Bench to Bedside #MMPMID27085376 Francis JM; Beck LH; Salant DJ Am J Kidney Dis 2016[Jul]; 68 (1): 138-47 PMID27085376show ga Lessons from an animal model that faithfully resembles human membranous nephropathy (MN) have informed our understanding of the pathogenesis of this organ-specific autoimmune disease and common cause of the nephrotic syndrome. Once it was established that the subepithelial immune deposits that characterize experimental MN form in situ when circulating antibodies bind to an intrinsic podocyte antigen, it was merely a matter of time before the human antigen was identified. The M-type phospholipase A2 receptor 1 (PLA2R) represents the major target antigen in primary MN, and thrombospondin type 1 domain-containing 7A (THSD7A) was more recently identified as a minor antigen. Serological tests for anti-PLA2R as well as kidney biopsy specimen staining for PLA2R exhibit more than 90% specificity and 70% to 80% sensitivity for the diagnosis of primary MN in most populations. The assays distinguish most cases of primary MN from MN associated with other systemic diseases, and sequential titers of anti-PLA2R are useful to monitor treatment response. A positive pre-transplantation test for anti-PLA2R is also helpful for predicting the risk of post-transplantation recurrence. Identification of target epitopes within PLA2R as well as the genetic association of primary MN with class II major histocompatibility and PLA2R1 variants are 2 additional examples of our evolving understanding of this disease. äMembranous Nephropathy: A Journey From Bench to Bedside (epmc).pdf DeepDyve Pubget Overpricing