• John A Kellum and Michael K Dishart.
• Department of Critical Care Medicine, University of Pittsburgh Medical Center, PA, USA. Kellumja@ccm.upmc.edu
• Crit Care. 2002 Oct 1; 6 (5): 429-33.

IntroductionHemofiltration may modulate the inflammatory response in sepsis through a variety of mechanisms. We sought to distinguish clearance from adsorption as the principal mechanism responsible for reducing circulating IL-6 levels with hemofiltration.Materials And MethodsNine hours after cecal ligation and puncture in 18 adult male Sprague-Dawley rats, we divided the rats into three groups (6 animals each) and placed groups 2 and 3 on a hemofiltration circuit connected between the right carotid artery and femoral vein using an AN69 membrane. In the hemofiltration group (group 2), ultrafiltrate was replaced with lactated Ringer's solution; in the recirculation group (group 3), the ultrafiltrate was reinfused into the animal. A sham group (group 1) had an arteriovenous circuit inserted but no hemofiltration. Blood was obtained for measurement of IL-6 and tumor necrosis factor (TNF) at the start of hemofiltration and after 5 and 11 hours of treatment.Results And DiscussionIL-6 levels increased only in the sham-treated animals (20.4 +/- 11.3 at baseline to 62.3 +/- 16.8 pg/ml at 11 hours, P = 0.03) (differences between groups 1 and 2, P = 0.015, and groups 1 and 3, P = 0.028). TNF levels were highly variable but not significantly different among the three groups.ConclusionHemofiltration-associated reductions in circulating IL-6 levels appear to be secondary to adsorption of mediators to the filter membrane. We do not know whether this is due to direct adsorption of IL-6 per se or to the absorption of other mediators with secondary downregulation of IL-6 production or release. In addition, we could not exclude an interaction between adsorption and hemofiltration.

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