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This Month in Anesthesiology  |   November 2000
Do Proinflammatory Cytokines Play a Role in Renal Dysfunction after Bypass?
Article Information
This Month in Anesthesiology
This Month in Anesthesiology   |   November 2000
Do Proinflammatory Cytokines Play a Role in Renal Dysfunction after Bypass?
Anesthesiology 11 2000, Vol.93, 5A. doi:
Anesthesiology 11 2000, Vol.93, 5A. doi:
Do Proinflammatory Cytokines Play a Role in Renal Dysfunction after Bypass? Gormley et al.(page 1210)
Gormley et al. recruited 20 patients scheduled to undergo coronary artery bypass grafting with use of cardiopulmonary bypass to measure changes in proinflammatory and antiinflammatory cytokines during surgery. Their aim was to determine whether there was a correlation between the magnitude of the plasma proinflammatory response and perioperative proximal tubular damage as measured by urinary N  -acetyl-β-[scap]d-glucosaminidase (NAG)/creatinine and α1-microglobulin/creatinine ratios.
Baseline blood samples were obtained before induction of anesthesia, after aortic cross-clamp release, and 2 and 24 h after termination of cardiopulmonary bypass. Urine samples were obtained at baseline, after aortic cross-clamp release, and 2, 6, 24, 48, and 72 h after termination of cardiopulmonary bypass. Plasma and urinary samples were assayed for the proinflammatory cytokines interleukin (IL)-1β, tumor necrosis factor (TNF) α, and IL-8 and for the antiinflammatory cytokines IL-10, IL-1 receptor antagonist (IL-1ra), and TNF soluble receptor 2 (TNFsr2). Urine also was assayed for NAG, creatinine, and α1-microglobulin.
After cardiopulmonary bypass, concentrations of plasma IL-8, IL-10, IL-1ra, and TNFsr2 were increased significantly compared with concentrations measured at baseline. Urinary IL-1ra, TNFsr2, NAG/creatinine and α1-microglobulin also were increased. The study showed a positive correlation between plasma TNFα concentrations at 2 h postoperatively and urinary NAG/creatinine ratios at 2 and 6 h postoperatively. Simultaneous with the increase in urinary IL-1ra and TNFsr2, there was a significant increase in proximal tubular dysfunction as indicated by increased urinary NAG/creatinine and α1-microglobulin/creatinine ratios. Although a direct causal relation is unlikely, what is likely is that a common mechanism may contribute both to the antiinflammatory cytokines in the urine and to the evidence of renal dysfunction. The authors suggest that the plasma proinflammatory cytokines, once filtered by the glomerulus, not only induce a degree of proximal tubular injury, but also trigger an intense intrarenal antiinflammatory response to allow the safe disposal of the proinflammatory cytokines. Thus, the kidney may be damaged by the inflammatory response it seeks to control.