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Volume 67, Issue 4, Pages 1216-1233 (April 2005)
IL-10, IL-6, and TNF-α: Central factors in the altered cytokine network of uremia—The good, the bad, and the ugly Peter Stenvinkel, Markus Ketteler, Richard J. Johnson, Bengt Lindholm, Roberto Pecoits-Filho, Miguel Riella, Olof Heimbürger, Tommy Cederholm, Matthias Girndt Kidney International Volume 67, Issue 4, Pages (April 2005) DOI: /j x Copyright © 2005 International Society of Nephrology Terms and Conditions
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Figure 1 Potential mechanisms by which pro- and anti-inflammatory cytokines may promote accelerated atherosclerosis, other uremic complications, and wasting. TNF-α is tumor necrosis factor-α; IL is interleukin. Kidney International , DOI: ( /j x) Copyright © 2005 International Society of Nephrology Terms and Conditions
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Figure 2 Inverse correlation between glomerular filtration rate and circulating interleukin-10 levels in a group of 151 end-stage renal disease patients starting dialysis treatment in Stockholm, Sweden. Kidney International , DOI: ( /j x) Copyright © 2005 International Society of Nephrology Terms and Conditions
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Figure 3 Proposed changes in body distribution (muscle mass and fat mass) and the atherosclerotic process in relation to interleukin-6 with increasing age in normal physiologic aging (top) and accelerated aging (bottom) observed in patients with wasting disorders, such as end-stage renal disease (ESRD), malignancy, congestive heart failure (CHF), rheumatoid arthritis (RA), and acquired immunodeficiency syndrome (AIDS). GFR is glomerular filtration rate; ICAM-1 is intercellular adhesion molecule-1; IL is interleukin. Kidney International , DOI: ( /j x) Copyright © 2005 International Society of Nephrology Terms and Conditions
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Figure 4 Simplified sketch of the interactions between pro- and anti-inflammatory cytokines and their inhibitors. Modifications of one factor in the network leads to compensatory alterations in many others, probably with the intention to make all activations temporary and regain a physiologic balance. IL is interleukin; TNF is tumor necrosis factor. Kidney International , DOI: ( /j x) Copyright © 2005 International Society of Nephrology Terms and Conditions
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Figure 5 Oversimplified sketch showing how the balance between Th1 and Th2 may be affected by genetic factors, retention of uremic solutes, immunomodulatory drugs [such as statins, glitazones and angiotensin-converting enzyme (ACE) inhibitors, environmental factors (such as infections, social hygiene and stress), and a vast number of diseases. IL is interleukin; TNF is tumor necrosis factor; INF is interferon; GN is glomerulonephritis; IDDM is insulin dependent diabetes mellitus; ESRD is end-stage renal disease. Kidney International , DOI: ( /j x) Copyright © 2005 International Society of Nephrology Terms and Conditions
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