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Dr. Diep D.Tran, Department of Surgery, University Hospital Groningen, Po Box 30.001, NL-9700 RB Groningen (The Netherlands) Dear Sir, Acute renal failure (ARF), particularly if associated with sepsis, other organ system failure, is a severe condition in critically ill patients and carries a mortality exceeding 60% [1,2]. Although prior chronic renal failure (CRF), sepsis and cardiopulmonary failure predispose to the development of ARF [2], outcome in ARF patients with CRF is paradoxically not worse or even better than in those without CRF in most studies [2,3], probably due to a lower prevalence of cardiovascular failure with hypotension and other sepsis-induced organ damage [2]. This protective effect of CRF can be explained in at least three different but not mutually exclusive ways. One possible explanation is given by Vi-jaykumar et al. [4] in a recent letter in Nephron. They found that most ARF patients with sepsis had high levels of plasma endotoxin, and in those without CRF a rise in antibodies to lipid-A (the most active component of endotoxin), probably as a consequence of translo-cation of gram-negative bacteria or endotoxin from the gut [5,6]. Patients with CRF, however, had already an accumulation of these antibodies before the development of ARF [4]. Since lipid-A acts as a primary signal for mononuclear and endothelial cells to release many biologically active factors that are responsible for the septic host response (tumor necrosis factor (TNF), interleukin-1 (IL-1), in-terleukin-6 (IL-6) and nitric oxide (NO)), exogenous antibodies directed against the lipid-A domain of endotoxin indeed significantly reduced mortality in patients with gram-negative bacteremia, particularly in those with concomitant shock and organ failure [7]. The second explanation involves inhibition of NO. NO is a potent vasodilator which is endogenously synthesized from L-arginine by two distinct NO synthase enzymes [8]. One of these NO synthases can be induced by endotoxin and cytokines such as TNF, and interleukins. This inducible enzyme is responsible for an excessive production of NO observed in various acute and chronic inflammatory conditions such as sepsis and inflammatory bowel disease [911], which has been implicated in the sustained hypotension, resistance to vasoconstrictors that are characteristic features of septic shock [9,10]. Furthermore, overproduction of NO may be cyto-toxic for target cells [8,12]. Inhibition of NO synthase by appropriate doses of specific inhibitors like N¤-monomethyl-L-arginine or NG-nitro-L-arginine-methyl ester results in an increase in blood pressure and systemic vascular resistance in animals and humans with septic shock [9,10]. Similarly, a rise in blood pressure was generated both in vitro and vivo by another

Possible Protective Effect of Chronic Renal Failure against Sepsis and Endotoxin-lnduced Organ Failure and Mortality in Acute Renal Failure