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British Journal of Anaesthesia, 2002, Vol. 88, No. 3 330-334
© 2002 The Board of Management and Trustees of the British Journal of Anaesthesia

Editorial

Editorial II

Role of the kidney in perioperative inflammatory responses

R. C. Baker1, M. A. Armstrong2, S. J. Allen3 and W. T. McBride3

1Department of Surgery The Queen’s University of Belfast Belfast UK 2Department of Immunobiology The Queen’s University of Belfast Belfast UK 3Department of Clinical Anaesthesia The Royal Group of Hospitals Trust Grosvenor Road Belfast BT12 6BA UK

Perioperative inflammatory responses are relatively well characterized. Increases in the plasma proinflammatory cytokines interleukin (IL)-1ß, tumour necrosis factor {alpha} (TNF-{alpha}) and IL-8 are later accompanied by increases in the anti-inflammatory cytokines IL-10, IL-1 receptor antagonist (IL-1ra) and TNF-{alpha} soluble receptors (TNF-sr)—the so-called phased anti-inflammatory response (PAIR).1–3 Proinflammatory cytokines act locally and in health are rarely detectable in plasma. In contrast, anti-inflammatory cytokines such as IL-1ra and TNF-sr are present in plasma in measurable concentrations. The molecular weights of IL-1ß, IL-8 and monomeric TNF-{alpha} are less than 20 kDa, rendering rapid glomerular filtration possible. As the biologically active form of TNF-{alpha} is a trimer (51 kDa) in equilibrium with the dimeric and monomeric forms, rapid filtration of the monomeric form may be expected to reduce the concentration of the biologically active trimer. This may be one reason why the proinflammatory cytokines are rarely detected in health and why, during an inflammatory response, their . . . [Full Text of this Article]

What happens to the control mechanism of the inflammatory response when the kidney starts to fail?

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