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10.1152/ajprenal.00456.2015 http://scihub22266oqcxt.onion/10.1152/ajprenal.00456.2015 C4967167!4967167!27147675     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2016 ; 311 (1): F120-30 Nephropedia Template TP {{tp|p=27147675|t=2016. Albumin contributes to kidney disease progression in Alport syndrome |pdf=|usr=}}{{27147675}} gab.com Text Albumin contributes to kidney disease progression in Alport syndrome JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27147675 #FOAvip Alport syndrome is a familial kidney disease caused by defects in the collagen type IV network of the glomerular basement membrane. Lack of collagen-?3?4?5(IV) changes the glomerular basement membrane morphologically and functionally, rendering it leaky to albumin and other plasma proteins. Filtered albumin has been suggested to be a cause of the glomerular and tubular injuries observed at advanced stages of Alport syndrome. To directly investigate the role that albumin plays in the progression of disease in Alport syndrome, we generated albumin knockout (Alb?/?) mice to use as a tool for removing albuminuria as a component of kidney disease. Mice lacking albumin were healthy and indistinguishable from control littermates, although they developed hypertriglyceridemia. Dyslipidemia was observed in Alb+/? mice, which displayed half the normal plasma albumin concentration. Alb mutant mice were bred to collagen-?3(IV) knockout (Col4a3?/?) mice, which are a model for human Alport syndrome. Lack of circulating and filtered albumin in Col4a3?/?;Alb?/? mice resulted in dramatically improved kidney disease outcomes, as these mice lived 64% longer than did Col4a3?/?;Alb+/+ and Col4a3?/?;Alb+/? mice, despite similar blood pressures and serum triglyceride levels. Further investigations showed that the absence of albumin correlated with reduced transforming growth factor-?1 signaling as well as reduced tubulointerstitial, glomerular, and podocyte pathology. We conclude that filtered albumin is injurious to kidney cells in Alport syndrome and perhaps in other proteinuric kidney diseases, including diabetic nephropathy. Twit Text FOAVip Albumin contributes to kidney disease progression in Alport syndrome ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27147675 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27147675 #FOAvip English Wikipedia <ref>{{Cite pmid|27147675}}</ref> Albumin contributes to kidney disease progression in Alport syndrome #MMPMID27147675 Jarad G; Knutsen RH; Mecham RP; Miner JH Am J Physiol Renal Physiol 2016[Jul]; 311 (1): F120-30 PMID27147675show ga Alport syndrome is a familial kidney disease caused by defects in the collagen type IV network of the glomerular basement membrane. Lack of collagen-?3?4?5(IV) changes the glomerular basement membrane morphologically and functionally, rendering it leaky to albumin and other plasma proteins. Filtered albumin has been suggested to be a cause of the glomerular and tubular injuries observed at advanced stages of Alport syndrome. To directly investigate the role that albumin plays in the progression of disease in Alport syndrome, we generated albumin knockout (Alb?/?) mice to use as a tool for removing albuminuria as a component of kidney disease. Mice lacking albumin were healthy and indistinguishable from control littermates, although they developed hypertriglyceridemia. Dyslipidemia was observed in Alb+/? mice, which displayed half the normal plasma albumin concentration. Alb mutant mice were bred to collagen-?3(IV) knockout (Col4a3?/?) mice, which are a model for human Alport syndrome. Lack of circulating and filtered albumin in Col4a3?/?;Alb?/? mice resulted in dramatically improved kidney disease outcomes, as these mice lived 64% longer than did Col4a3?/?;Alb+/+ and Col4a3?/?;Alb+/? mice, despite similar blood pressures and serum triglyceride levels. Further investigations showed that the absence of albumin correlated with reduced transforming growth factor-?1 signaling as well as reduced tubulointerstitial, glomerular, and podocyte pathology. We conclude that filtered albumin is injurious to kidney cells in Alport syndrome and perhaps in other proteinuric kidney diseases, including diabetic nephropathy. äAlbumin contributes to kidney disease progression in Alport syndrome (epmc).pdf DeepDyve Pubget Overpricing