4.6 Article Proceedings Paper

Plasma and urinary cytokine homeostasis and renal dysfunction during cardiac surgery

Journal

ANESTHESIOLOGY
Volume 93, Issue 5, Pages 1210-1216

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00000542-200011000-00013

Keywords

cardiopulmonary bypass; proximal tubule

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Background Cardiac surgery induces changes in plasma cytokines, Proinflammatory cytokines have been associated with a number of renal diseases. The proinflammatory cytokines interleukin 8 (IL-8), tumor necrosis factor alpha (TNF alpha), and interleukin 1 beta (IL-1 beta) are smaller than the antiinflammatory cytokines Interleukin 10 (IL-10), interleukin 1 receptor antagonist (IL-1ra), and TNF soluble receptor 2 (TNFsr2), and thus undergo glomerular filtration more readily. Accordingly, this study investigated the relation between plasma and urinary cytokines and proximal renal dysfunction during cardiac surgery. Methods:Twenty patients undergoing coronary artery bypass grafting with cardiopulmonary bypass (CPB) were studied. Blood and urine samples were analyzed for proinflammatory and antiinflammatory cytokines, Proximal tubular dysfunction was measured using urinary N-acetyl-beta -D-glucosaminidase (NAG)/creatinine and alpha (1)-microglobulin/creatinine ratios. Results: Plasma IL-8, IL-10, IL-1ra, and TNFsr2 values were significantly elevated compared with baseline. Urinary IL-1ra and TNFsr2 were significantly elevated. Urinary NAG/creatinine and alpha (1)-microglobulin/creatinine ratios were also elevated. Plasma TNF alpha at 2 h correlated with urinary NAG/creatinine ratio at 2 and 6 h (P < 0.05) and with urinary IL-1ra at 2 h (P < 0.05), Plasma IL-8 at 2 h correlated with NAG/creatinine at 6 h (P < 0.05). Urinary IL-1ra correlated with urinary NAG/creatinine ratio after cross-clamp release and 2 and 6 h after CPB (P < 0.05), Conclusions: Cardiac surgery using CPB leads to changes in plasma and urinary cytokine homeostasis that correlate with renal proximal tubular dysfunction, This dysfunction may be related to the renal filtration of proinflammatory mediators. Renal autoprotective mechanisms may involve the intrarenal generation of antiinflammatory cytokines.

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