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10.1371/journal.pone.0155255 http://scihub22266oqcxt.onion/10.1371/journal.pone.0155255 C4871445!4871445!27192434     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27192434.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+One 2016 ; 11 (5): ä Nephropedia Template TP {{tp|p=27192434|t=2016. Podocyte Depletion in Thin GBM and Alport Syndrome |pdf=|usr=}}{{27192434}} gab.com Text Podocyte Depletion in Thin GBM and Alport Syndrome JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27192434 #FOAvip The proximate genetic cause of both Thin GBM and Alport Syndrome (AS) is abnormal ?3, 4 and 5 collagen IV chains resulting in abnormal glomerular basement membrane (GBM) structure/function. We previously reported that podocyte detachment rate measured in urine is increased in AS, suggesting that podocyte depletion could play a role in causing progressive loss of kidney function. To test this hypothesis podometric parameters were measured in 26 kidney biopsies from 21 patients aged 2?17 years with a clinic-pathologic diagnosis including both classic Alport Syndrome with thin and thick GBM segments and lamellated lamina densa [n = 15] and Thin GBM cases [n = 6]. Protocol biopsies from deceased donor kidneys were used as age-matched controls. Podocyte depletion was present in AS biopsies prior to detectable histologic abnormalities. No abnormality was detected by light microscopy at <30% podocyte depletion, minor pathologic changes (mesangial expansion and adhesions to Bowman?s capsule) were present at 30?50% podocyte depletion, and FSGS was progressively present above 50% podocyte depletion. eGFR did not change measurably until >70% podocyte depletion. Low level proteinuria was an early event at about 25% podocyte depletion and increased in proportion to podocyte depletion. These quantitative data parallel those from model systems where podocyte depletion is the causative event. This result supports a hypothesis that in AS podocyte adherence to the GBM is defective resulting in accelerated podocyte detachment causing progressive podocyte depletion leading to FSGS-like pathologic changes and eventual End Stage Kidney Disease. Early intervention to reduce podocyte depletion is projected to prolong kidney survival in AS. Twit Text FOAVip Podocyte Depletion in Thin GBM and Alport Syndrome ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27192434 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27192434 #FOAvip English Wikipedia <ref>{{Cite pmid|27192434}}</ref> Podocyte Depletion in Thin GBM and Alport Syndrome #MMPMID27192434 Wickman L; Hodgin JB; Wang SQ; Afshinnia F; Kershaw D; Wiggins RC PLoS One 2016[]; 11 (5): ä PMID27192434show ga The proximate genetic cause of both Thin GBM and Alport Syndrome (AS) is abnormal ?3, 4 and 5 collagen IV chains resulting in abnormal glomerular basement membrane (GBM) structure/function. We previously reported that podocyte detachment rate measured in urine is increased in AS, suggesting that podocyte depletion could play a role in causing progressive loss of kidney function. To test this hypothesis podometric parameters were measured in 26 kidney biopsies from 21 patients aged 2?17 years with a clinic-pathologic diagnosis including both classic Alport Syndrome with thin and thick GBM segments and lamellated lamina densa [n = 15] and Thin GBM cases [n = 6]. Protocol biopsies from deceased donor kidneys were used as age-matched controls. Podocyte depletion was present in AS biopsies prior to detectable histologic abnormalities. No abnormality was detected by light microscopy at <30% podocyte depletion, minor pathologic changes (mesangial expansion and adhesions to Bowman?s capsule) were present at 30?50% podocyte depletion, and FSGS was progressively present above 50% podocyte depletion. eGFR did not change measurably until >70% podocyte depletion. Low level proteinuria was an early event at about 25% podocyte depletion and increased in proportion to podocyte depletion. These quantitative data parallel those from model systems where podocyte depletion is the causative event. This result supports a hypothesis that in AS podocyte adherence to the GBM is defective resulting in accelerated podocyte detachment causing progressive podocyte depletion leading to FSGS-like pathologic changes and eventual End Stage Kidney Disease. Early intervention to reduce podocyte depletion is projected to prolong kidney survival in AS. äPodocyte Depletion in Thin GBM and Alport Syndrome (epmc).pdf DeepDyve Pubget Overpricing