The Experts below are selected from a list of 8319 Experts worldwide ranked by ideXlab platform
Henry Punzi - One of the best experts on this subject based on the ideXlab platform.
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urine markers of Kidney Tubule Cell injury and Kidney function decline in sprint trial participants with ckd
Clinical Journal of The American Society of Nephrology, 2020Co-Authors: Rakesh Malhotra, Walter T. Ambrosius, Alfred K. Cheung, Vasantha Jotwani, Ronit Katz, Kalani L Raphael, William E Haley, Anjay Rastogi, Barry I Freedman, Henry PunziAbstract:Background and objectives eGFR and albuminuria primarily reflect glomerular function and injury, whereas Tubule Cell atrophy and interstitial fibrosis on Kidney biopsy are important risk markers for CKD progression. Kidney Tubule injury markers have primarily been studied in hospitalized AKI. Here, we examined the association between urinary Kidney Tubule injury markers at baseline with subsequent loss of Kidney function in persons with nondiabetic CKD who participated in the Systolic Blood Pressure Intervention Trial (SPRINT). Design, setting, participants, & measurements Among 2428 SPRINT participants with CKD (eGFR Results Mean participant age was 73±9 (SD) years, 60% were men, 66% were white, and mean baseline eGFR was 46±11 ml/min per 1.73 m2. There were 87 Kidney composite outcome events during a median follow-up of 3.8 years. Relative to the respective lowest quartiles, the highest quartiles of urinary KIM-1 (hazard ratio, 2.84; 95% confidence interval [95% CI], 1.31 to 6.17), MCP-1 (hazard ratio, 2.43; 95% CI, 1.13 to 5.23), and YKL-40 (hazard ratio, 1.95; 95% CI, 1.08 to 3.51) were associated with higher risk of the Kidney composite outcome in fully adjusted models including baseline eGFR and urine albumin. In linear analysis, urinary IL-18 was the only marker associated with eGFR decline (−0.91 ml/min per 1.73 m2 per year for highest versus lowest quartile; 95% CI, −1.44 to −0.38), a finding that was stronger in the standard arm of SPRINT. Conclusions Urine markers of Tubule Cell injury provide information about risk of subsequent loss of Kidney function, beyond the eGFR and urine albumin.
Rakesh Malhotra - One of the best experts on this subject based on the ideXlab platform.
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urine markers of Kidney Tubule Cell injury and Kidney function decline in sprint trial participants with ckd
Clinical Journal of The American Society of Nephrology, 2020Co-Authors: Rakesh Malhotra, Walter T. Ambrosius, Alfred K. Cheung, Vasantha Jotwani, Ronit Katz, Kalani L Raphael, William E Haley, Anjay Rastogi, Barry I Freedman, Henry PunziAbstract:Background and objectives eGFR and albuminuria primarily reflect glomerular function and injury, whereas Tubule Cell atrophy and interstitial fibrosis on Kidney biopsy are important risk markers for CKD progression. Kidney Tubule injury markers have primarily been studied in hospitalized AKI. Here, we examined the association between urinary Kidney Tubule injury markers at baseline with subsequent loss of Kidney function in persons with nondiabetic CKD who participated in the Systolic Blood Pressure Intervention Trial (SPRINT). Design, setting, participants, & measurements Among 2428 SPRINT participants with CKD (eGFR Results Mean participant age was 73±9 (SD) years, 60% were men, 66% were white, and mean baseline eGFR was 46±11 ml/min per 1.73 m2. There were 87 Kidney composite outcome events during a median follow-up of 3.8 years. Relative to the respective lowest quartiles, the highest quartiles of urinary KIM-1 (hazard ratio, 2.84; 95% confidence interval [95% CI], 1.31 to 6.17), MCP-1 (hazard ratio, 2.43; 95% CI, 1.13 to 5.23), and YKL-40 (hazard ratio, 1.95; 95% CI, 1.08 to 3.51) were associated with higher risk of the Kidney composite outcome in fully adjusted models including baseline eGFR and urine albumin. In linear analysis, urinary IL-18 was the only marker associated with eGFR decline (−0.91 ml/min per 1.73 m2 per year for highest versus lowest quartile; 95% CI, −1.44 to −0.38), a finding that was stronger in the standard arm of SPRINT. Conclusions Urine markers of Tubule Cell injury provide information about risk of subsequent loss of Kidney function, beyond the eGFR and urine albumin.
Patricia I Oteiza - One of the best experts on this subject based on the ideXlab platform.
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aldosterone increases Kidney Tubule Cell oxidants through calcium mediated activation of nadph oxidase and nitric oxide synthase
Free Radical Biology and Medicine, 2011Co-Authors: Nina Queisser, Nicole Schupp, Helga Stopper, Reinhard Schinzel, Patricia I OteizaAbstract:Abstract Chronic hyperaldosteronism has been associated with an increased cancer risk. We recently showed that aldosterone causes an increase in Cell oxidants, DNA damage, and NF-κB activation. This study investigated the mechanisms underlying aldosterone-induced increase in Cell oxidants in Kidney Tubule Cells. Aldosterone caused an increase in both reactive oxygen and reactive nitrogen (RNS) species. The involvement of the activation of NADPH oxidase in the increase in Cellular oxidants was demonstrated by the inhibitory action of the NADPH oxidase inhibitors DPI, apocynin, and VAS2870 and by the migration of the p47 subunit to the membrane. NADPH oxidase activation occurred as a consequence of an increase in Cellular calcium levels and was mediated by protein kinase C. The prevention of RNS increase by BAPTA-AM, W-7, and L-NAME indicates a calcium–calmodulin activation of NOS. A similar pattern of effects of the NADPH oxidase and NOS inhibitors was observed for aldosterone-induced DNA damage and NF-κB activation, both central to the pathogenesis of chronic aldosteronism. In summary, this paper demonstrates that aldosterone, via the mineralocorticoid receptor, causes an increase in Kidney Cell oxidants, DNA damage, and NF-κB activation through a calcium-mediated activation of NADPH oxidase and NOS. Therapies targeting calcium, NOS, and NADPH oxidase could prevent the adverse effects of hyperaldosteronism on Kidney function as well as its potential oncogenic action.
Anjay Rastogi - One of the best experts on this subject based on the ideXlab platform.
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urine markers of Kidney Tubule Cell injury and Kidney function decline in sprint trial participants with ckd
Clinical Journal of The American Society of Nephrology, 2020Co-Authors: Rakesh Malhotra, Walter T. Ambrosius, Alfred K. Cheung, Vasantha Jotwani, Ronit Katz, Kalani L Raphael, William E Haley, Anjay Rastogi, Barry I Freedman, Henry PunziAbstract:Background and objectives eGFR and albuminuria primarily reflect glomerular function and injury, whereas Tubule Cell atrophy and interstitial fibrosis on Kidney biopsy are important risk markers for CKD progression. Kidney Tubule injury markers have primarily been studied in hospitalized AKI. Here, we examined the association between urinary Kidney Tubule injury markers at baseline with subsequent loss of Kidney function in persons with nondiabetic CKD who participated in the Systolic Blood Pressure Intervention Trial (SPRINT). Design, setting, participants, & measurements Among 2428 SPRINT participants with CKD (eGFR Results Mean participant age was 73±9 (SD) years, 60% were men, 66% were white, and mean baseline eGFR was 46±11 ml/min per 1.73 m2. There were 87 Kidney composite outcome events during a median follow-up of 3.8 years. Relative to the respective lowest quartiles, the highest quartiles of urinary KIM-1 (hazard ratio, 2.84; 95% confidence interval [95% CI], 1.31 to 6.17), MCP-1 (hazard ratio, 2.43; 95% CI, 1.13 to 5.23), and YKL-40 (hazard ratio, 1.95; 95% CI, 1.08 to 3.51) were associated with higher risk of the Kidney composite outcome in fully adjusted models including baseline eGFR and urine albumin. In linear analysis, urinary IL-18 was the only marker associated with eGFR decline (−0.91 ml/min per 1.73 m2 per year for highest versus lowest quartile; 95% CI, −1.44 to −0.38), a finding that was stronger in the standard arm of SPRINT. Conclusions Urine markers of Tubule Cell injury provide information about risk of subsequent loss of Kidney function, beyond the eGFR and urine albumin.
Alfred K. Cheung - One of the best experts on this subject based on the ideXlab platform.
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urine markers of Kidney Tubule Cell injury and Kidney function decline in sprint trial participants with ckd
Clinical Journal of The American Society of Nephrology, 2020Co-Authors: Rakesh Malhotra, Walter T. Ambrosius, Alfred K. Cheung, Vasantha Jotwani, Ronit Katz, Kalani L Raphael, William E Haley, Anjay Rastogi, Barry I Freedman, Henry PunziAbstract:Background and objectives eGFR and albuminuria primarily reflect glomerular function and injury, whereas Tubule Cell atrophy and interstitial fibrosis on Kidney biopsy are important risk markers for CKD progression. Kidney Tubule injury markers have primarily been studied in hospitalized AKI. Here, we examined the association between urinary Kidney Tubule injury markers at baseline with subsequent loss of Kidney function in persons with nondiabetic CKD who participated in the Systolic Blood Pressure Intervention Trial (SPRINT). Design, setting, participants, & measurements Among 2428 SPRINT participants with CKD (eGFR Results Mean participant age was 73±9 (SD) years, 60% were men, 66% were white, and mean baseline eGFR was 46±11 ml/min per 1.73 m2. There were 87 Kidney composite outcome events during a median follow-up of 3.8 years. Relative to the respective lowest quartiles, the highest quartiles of urinary KIM-1 (hazard ratio, 2.84; 95% confidence interval [95% CI], 1.31 to 6.17), MCP-1 (hazard ratio, 2.43; 95% CI, 1.13 to 5.23), and YKL-40 (hazard ratio, 1.95; 95% CI, 1.08 to 3.51) were associated with higher risk of the Kidney composite outcome in fully adjusted models including baseline eGFR and urine albumin. In linear analysis, urinary IL-18 was the only marker associated with eGFR decline (−0.91 ml/min per 1.73 m2 per year for highest versus lowest quartile; 95% CI, −1.44 to −0.38), a finding that was stronger in the standard arm of SPRINT. Conclusions Urine markers of Tubule Cell injury provide information about risk of subsequent loss of Kidney function, beyond the eGFR and urine albumin.
