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10.1186/s12953-016-0096-7 http://scihub22266oqcxt.onion/10.1186/s12953-016-0096-7 C4807542!4807542!27019641     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Proteome+Sci 2016 ; 14 (ä): ä Nephropedia Template TP {{tp|p=27019641|t=2016. The association of plasma cystatin C proteoforms with diabetic chronic kidney disease |pdf=|usr=}}{{27019641}} gab.com Text The association of plasma cystatin C proteoforms with diabetic chronic kidney disease JO: Proteome Sci http://www.kidney.de/pget.php?&tw=1&pmid=27019641 #FOAvip Background: Cystatin C (CysC) is an endogenous cysteine protease inhibitor that can be used to assess the progression of kidney function. Recent studies demonstrate that CysC is a more specific indicator of glomerular filtration rate (GFR) than creatinine. CysC in plasma exists in multiple proteoforms. The goal of this study was to clarify the association of native CysC, CysC missing N-terminal Serine (CysC des-S), and CysC without three N-terminal residues (CysC des-SSP) with diabetic chronic kidney disease (CKD). Results: Using mass spectrometric immunoassay, the plasma concentrations of native CysC and the two CysC truncation proteoforms were examined in 111 individuals from three groups: 33 non-diabetic controls, 34 participants with type 2 diabetes (DM) and without CKD and 44 participants with diabetic CKD. Native CysC concentrations were 1.4 fold greater in CKD compared to DM group (p?=?0.02) and 1.5 fold greater in CKD compared to the control group (p?=?0.001). CysC des-S concentrations were 1.55 fold greater in CKD compared to the DM group (p?=?0.002) and 1.9 fold greater in CKD compared to the control group (p?=?0.0002). CysC des-SSP concentrations were 1.8 fold greater in CKD compared to the DM group (p?=?0.008) and 1.52 fold greater in CKD compared to the control group (p?=?0.002). In addition, the concentrations of CysC proteoforms were greater in the setting of albuminuria. The truncated CysC proteoform concentrations were associated with estimated GFR independent of native CysC concentrations. Conclusion: Our findings demonstrate a greater amount of CysC proteoforms in diabetic CKD. We therefore suggest assessing the role of cystatin C proteoforms in the progression of CKD. Electronic supplementary material: The online version of this article (doi:10.1186/s12953-016-0096-7) contains supplementary material, which is available to authorized users. Twit Text FOAVip The association of plasma cystatin C proteoforms with diabetic chronic kidney disease ????Proteome Sci http://www.kidney.de/pget.php?&tw=1&pmid=27019641 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27019641 #FOAvip English Wikipedia <ref>{{Cite pmid|27019641}}</ref> The association of plasma cystatin C proteoforms with diabetic chronic kidney disease #MMPMID27019641 Yassine HN; Trenchevska O; Dong Z; Bashawri Y; Koska J; Reaven PD; Nelson RW; Nedelkov D Proteome Sci 2016[]; 14 (ä): ä PMID27019641show ga Background: Cystatin C (CysC) is an endogenous cysteine protease inhibitor that can be used to assess the progression of kidney function. Recent studies demonstrate that CysC is a more specific indicator of glomerular filtration rate (GFR) than creatinine. CysC in plasma exists in multiple proteoforms. The goal of this study was to clarify the association of native CysC, CysC missing N-terminal Serine (CysC des-S), and CysC without three N-terminal residues (CysC des-SSP) with diabetic chronic kidney disease (CKD). Results: Using mass spectrometric immunoassay, the plasma concentrations of native CysC and the two CysC truncation proteoforms were examined in 111 individuals from three groups: 33 non-diabetic controls, 34 participants with type 2 diabetes (DM) and without CKD and 44 participants with diabetic CKD. Native CysC concentrations were 1.4 fold greater in CKD compared to DM group (p?=?0.02) and 1.5 fold greater in CKD compared to the control group (p?=?0.001). CysC des-S concentrations were 1.55 fold greater in CKD compared to the DM group (p?=?0.002) and 1.9 fold greater in CKD compared to the control group (p?=?0.0002). CysC des-SSP concentrations were 1.8 fold greater in CKD compared to the DM group (p?=?0.008) and 1.52 fold greater in CKD compared to the control group (p?=?0.002). In addition, the concentrations of CysC proteoforms were greater in the setting of albuminuria. The truncated CysC proteoform concentrations were associated with estimated GFR independent of native CysC concentrations. Conclusion: Our findings demonstrate a greater amount of CysC proteoforms in diabetic CKD. We therefore suggest assessing the role of cystatin C proteoforms in the progression of CKD. Electronic supplementary material: The online version of this article (doi:10.1186/s12953-016-0096-7) contains supplementary material, which is available to authorized users. äThe association of plasma cystatin C proteoforms with diabetic chronic(epmc).pdf DeepDyve Pubget Overpricing