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10.1097/MAJ.0b013e3182a5b6dd http://scihub22266oqcxt.onion/10.1097/MAJ.0b013e3182a5b6dd C4000293!4000293 !24165783     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24165783 &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 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24165783 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Med+Sci 2014 ; 348 (4 ): 306-14 Nephropedia Template TP {{tp|p=24165783 |t=2014. Renoprotective effects of direct renin inhibition in glomerulonephritis |pdf=|usr=}}{{24165783 }} gab.com Text Renoprotective effects of direct renin inhibition in glomerulonephritis JO: Am J Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=24165783 #FOAvip The development of glomerulonephritis causes glomerular injury and renal dysfunction and is thought to increase renin release, thus activating the renin-angiotensin system (RAS). The aims of this study were to demonstrate activation of the intrarenal RAS and determine the effects of direct renin inhibition (DRI) on the progression of glomerulonephritis. Rats were treated with anti-Thy1.1 antibody with or without DRI, aliskiren (30 mg/kg/d). In the glomerulonephritic rats, protein, microalbumin excretion levels, urinary angiotensinogen excretion, glomerular expansion score and intrarenal transforming growth factor-? and plasminogen activator inhibitor-1 mRNA levels were augmented compared with control rats; however, hypertension was not observed in the glomerulonephritic rats, and aliskiren treatment did not modify their blood pressure. The increases in urinary protein (94.7 ± 13.0 mg/d) and microalbumin (7.52 ± 2.6 mg/d) excretion were reduced by aliskiren (43.6 ± 4.5 mg/d of protein and 2.57 ± 0.7 mg/d of microalbumin). Furthermore, the progression of glomerular expansion and elevation of intrarenal transforming growth factor-? and plasminogen activator inhibitor-1 levels were prevented by aliskiren. Importantly, aliskiren suppressed the augmentation of urinary angiotensinogen levels, the increased angiotensinogen expression in the kidneys and the increases in Ang II levels in renal medulla induced by the anti-Thy1.1 antibody. These results suggest that DRI with aliskiren prevents intrarenal RAS activation leading to mitigation of the development of glomerulonephritis. In addition, the renoprotective effects of DRI on glomerulonephritis occur in a blood pressure-independent manner. Accordingly, treatment with aliskiren may be an effective approach to treat glomerulonephritis and other intrarenal RAS-associated kidney diseases. Twit Text FOAVip Renoprotective effects of direct renin inhibition in glomerulonephritis ????Am J Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=24165783 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24165783 #FOAvip English Wikipedia <ref>{{Cite pmid|24165783 }}</ref> Renoprotective effects of direct renin inhibition in glomerulonephritis #MMPMID24165783 Miyata K ; Satou R ; Inui D ; Katsurada A ; Seth D ; Davis A ; Urushihara M ; Kobori H ; Mitchell KD ; Navar LG Am J Med Sci 2014[Oct]; 348 (4 ): 306-14 PMID24165783 show ga The development of glomerulonephritis causes glomerular injury and renal dysfunction and is thought to increase renin release, thus activating the renin-angiotensin system (RAS). The aims of this study were to demonstrate activation of the intrarenal RAS and determine the effects of direct renin inhibition (DRI) on the progression of glomerulonephritis. Rats were treated with anti-Thy1.1 antibody with or without DRI, aliskiren (30 mg/kg/d). In the glomerulonephritic rats, protein, microalbumin excretion levels, urinary angiotensinogen excretion, glomerular expansion score and intrarenal transforming growth factor-? and plasminogen activator inhibitor-1 mRNA levels were augmented compared with control rats; however, hypertension was not observed in the glomerulonephritic rats, and aliskiren treatment did not modify their blood pressure. The increases in urinary protein (94.7 ± 13.0 mg/d) and microalbumin (7.52 ± 2.6 mg/d) excretion were reduced by aliskiren (43.6 ± 4.5 mg/d of protein and 2.57 ± 0.7 mg/d of microalbumin). Furthermore, the progression of glomerular expansion and elevation of intrarenal transforming growth factor-? and plasminogen activator inhibitor-1 levels were prevented by aliskiren. Importantly, aliskiren suppressed the augmentation of urinary angiotensinogen levels, the increased angiotensinogen expression in the kidneys and the increases in Ang II levels in renal medulla induced by the anti-Thy1.1 antibody. These results suggest that DRI with aliskiren prevents intrarenal RAS activation leading to mitigation of the development of glomerulonephritis. In addition, the renoprotective effects of DRI on glomerulonephritis occur in a blood pressure-independent manner. Accordingly, treatment with aliskiren may be an effective approach to treat glomerulonephritis and other intrarenal RAS-associated kidney diseases. |Amides/pharmacology/*therapeutic use [MESH] |Animals [MESH] |Fumarates/pharmacology/*therapeutic use [MESH] |Glomerulonephritis/*metabolism/*prevention & control [MESH] |Kidney Glomerulus/drug effects/metabolism [MESH] |Male [MESH] |Rats [MESH] |Rats, Inbred F344 [MESH] |Rats, Sprague-Dawley [MESH] |Renin-Angiotensin System/drug effects/physiology [MESH] |Renin/*antagonists & inhibitors/*metabolism [MESH]Renoprotective effects of direct renin inhibition in glomerulonephriti(epmc).pdf DeepDyve Pubget Overpricing