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220 klenzak & himmelfarb renal tubule-assist device, and then infused with endotoxin. Again, IL-10 levels were higher in the renal tubule-assist device–treated group, as was mean arterial pressure. Survival data were not published [39]. To assess whether the renal tubule-assist device ameliorates the course of sepsis before renal failure, the investigators assessed it in pigs administered E. coli intraperitoneally, which were immediately started on CVVHF with or without renal tubule-assist device. All of the animals developed ARF within hours. This study demonstrated a significant increase in survival time, associated with better systemic hemodynamic measurements and renal artery blood flow. IL-6 and interferon-g levels were lower in renal tubule-assist device–treated animals, but most cytokines measured did not demonstrate significant differences between renal tubule-assist device and sham-treated animals [40]. Summary When renal failure occurs, the systemic and local dysregulation of sepsis is compounded by loss of metabolic, fluid, and electrolyte homeostasis. The loss of renal function increases mortality, and those who do survive likely do so with the return of renal function. The interplay between systemic host responses and local injury and activity in the kidney affects the vascular bed, the immune system, and plays a role in the development of MOSF. Patients with end-stage renal disease and sepsis have a lower mortality rate than those who develop ARF in the setting of sepsis. Despite advances in RRT and critical care, mortality rates have remained fairly stable over the last two decades for sepsis-associated ARF. There is little conclusive evidence from human trials of great benefit from the myriad of original therapies tested to date. For these reasons, it is important to learn more about the human response to sepsis and ARF, and to clarify the differences between patients who develop renal failure and those who do not; and to clarify the differences between those who survive, and those who do not. It is these variables, in the ICU, which may serve to aid in designing rational therapies for the restoration of metabolic balance and the return of renal function. References [1] Rangel-Frausto MS, Pittet D, Costigan M, et al. The natural history of the systemic inflammatory response syndrome (SIRS): a prospective study. JAMA 1995;273:117–23. [2] Clermont G, Acker CG, Angus DC, et al. Renal failure in the ICU: comparison of the impact of acute renal failure and end-stage renal disease on ICU outcomes. Kidney Int 2002;62:986–96. [3] Lugon JR, Boim MA, Ramos OL, et al. Renal function and glomerular hemodynamics in male endotoxemic rats. Kidney Int 1989;36:570–5. [4] Kashgarian M, Siegel NJ, Ries AL, et al. Hemodynamic aspects in development and recovery phases of experimental postischemic acute renal failure. Kidney Int Suppl 1976;6:S160–8.
sepsis and the kidney 221 [5] Mason J, Torhorst J, Welsch J. Role of the medullary perfusion defect in the pathogenesis of ischemic renal failure. Kidney Int 1984;26:283–93. [6] Wan L, Bellomo R, Di GD, et al. The pathogenesis of septic acute renal failure. Curr Opin Crit Care 2003;9:496–502. [7] Schaer GL, Fink MP, Parrillo JE. Norepinephrine alone versus norepinephrine plus low-dose dopamine: enhanced renal blood flow with combination pressor therapy. Crit Care Med 1985; 13:492–6. [8] Anderson WP, Korner PI, Selig SE. Mechanisms involved in the renal responses to intravenous and renal artery infusions of noradrenaline in conscious dogs. J Physiol 1981;32:121–30. [9] Korner PI, Stokes GS, White SW, et al. Role of the autonomic nervous system in the renal vasoconstriction response to hemorrhage in the rabbit. Circ Res 1967;20:676–85. [10] Zhang H, Smail N, Cabral A, et al. Effects of norepinephrine on regional blood flow and oxygen extraction capabilities during endotoxic shock. Am J Respir Crit Care Med 1997;155:1965 –71. [11] Bersten AD, Rutten AJ. Renovascular interaction of epinephrine, dopamine, and intraperitoneal sepsis. Crit Care Med 1995;23:537– 44. [12] Bersten AD, Rutten AJ, Summersides G, et al. Epinephrine infusion in sheep: systemic and renal hemodynamic effects. Crit Care Med 1994;22:994–1001. [13] Di GD, Morimatsu H, May CN, et al. Intrarenal blood flow distribution in hyperdynamic septic shock: effect of norepinephrine. Crit Care Med 2003;31:2509–13. [14] Cohen RI, Hassell AM, Marzouk K, et al. Renal effects of nitric oxide in endotoxemia. Am J Respir Crit Care Med 2001;164(10 Pt 1):1890–5. [15] Spain DA, Wilson MA, Garrison RN. Nitric oxide synthase inhibition exacerbates sepsisinduced renal hypoperfusion. Surgery 1994;116:322–30. [16] Knotek M, Esson M, Gengaro P, et al. Desensitization of soluble guanylate cyclase in renal cortex during endotoxemia in mice. J Am Soc Nephrol 2000;11:2133–7. [17] Zimmerman GA, Prescott SM, McIntyre TM. Endothelial cell interactions with granulocytes: tethering and signaling molecules. Immunol Today 1992;13:93 – 100. [18] Shimizu T, Kuroda T, Ikeda M, et al. Potential contribution of endothelin to renal abnormalities in glycerol-induced acute renal failure in rats. J Pharmacol Exp Ther 1998;286:977–83. [19] Forbes JM, Hewitson TD, Becker GJ, et al. Simultaneous blockade of endothelin A and B receptors in ischemic acute renal failure is detrimental to long-term kidney function. Kidney Int 2001;59:1333– 41. [20] Thijs A, Thijs LG. Pathogenesis of renal failure in sepsis. Kidney Int Suppl 1998;66:S34–7. [21] Kohan DE. Role of endothelin and tumour necrosis factor in the renal response to sepsis. Nephrol Dial Transplant 1994;9(Suppl 4):73–7. [22] Linas SL, Whittenburg D, Parsons PE, et al. Ischemia increases neutrophil retention and worsens acute renal failure: role of oxygen metabolites and ICAM 1. Kidney Int 1995;48:1584–91. [23] Camussi G, Ronco C, Montrucchio G, et al. Role of soluble mediators in sepsis and renal failure. Kidney Int Suppl 1998;66:S38– 42. [24] Xia Y, Feng L, Yoshimura T, et al. LPS-induced MCP-1, IL-1 beta, and TNF-alpha mRNA expression in isolated erythrocyte-perfused rat kidney. Am J Physiol 1993;264(5 Pt 2):F774–80. [25] Linas SL, Whittenburg D, Repine JE. Role of neutrophil derived oxidants and elastase in lipopolysaccharide-mediated renal injury. Kidney Int 1991;39:618–23. [26] Wang J, Dunn MJ. Platelet-activating factor mediates endotoxin-induced acute renal insufficiency in rats. Am J Physiol 1987;253(6 Pt 2):F1283–9. [27] Himmelfarb J, McMonagle E, Freedman S, et al. Oxidative stress is increased in critically ill patients with acute renal failure. J Am Soc Nephrol 2004;15:2449–56. [28] Carraway MS, Welty-Wolf KE, Miller DL, et al. Blockade of tissue factor: treatment for organ injury in established sepsis. Am J Respir Crit Care Med 2003;167:1200 – 9. [29] Bernard GR, Vincent JL, Laterre PF, et al. Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med 2001;344:699–709. [30] Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet 2000; 356:26–30.
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