Urinary Indices and Microscopy in Sepsis-Related Acute Renal Failure Robert W. Schrier, MD  American Journal of Kidney Diseases  Volume 48, Issue 5, Pages 838-841 (November 2006) DOI: 10.1053/j.ajkd.2006.08.024 Copyright © 2006 National Kidney Foundation, Inc. Terms and Conditions

Fig 1 Arterial vasodilatation and renal vasoconstriction in patients with sepsis. Endotoxemia stimulates the induction of nitric oxide synthase, which leads to nitric oxide–mediated arterial vasodilatation. The resultant arterial underfilling is sensed by the baroreceptors and results in an increase in sympathetic outflow and the release of arginine vasopressin (AVP) from the central nervous system, with activation of the renin-angiotensin-aldosterone system (RAAS). The increases in sympathetic and angiotensin activities lead to renal vasoconstriction, which predisposes to ARF. Reprinted with permission from Schrier and Wang.3 American Journal of Kidney Diseases 2006 48, 838-841DOI: (10.1053/j.ajkd.2006.08.024) Copyright © 2006 National Kidney Foundation, Inc. Terms and Conditions

Fig 2 FeNa during endotoxemia in awake rats. Endotoxemia treatment increased tubular sodium reabsorption and decreased FeNa during the first hour (prerenal azotemia). Prolonged effects of endotoxemia were associated with tubular damage and increases in FeNa as rats developed ATN. Reprinted with permission from Kikeri et al.5 American Journal of Kidney Diseases 2006 48, 838-841DOI: (10.1053/j.ajkd.2006.08.024) Copyright © 2006 National Kidney Foundation, Inc. Terms and Conditions

Fig 3 Schema of pathogenetic sites for therapeutic interventions during sepsis and endotoxemia. Use of arginine vasopressin (AVP), hydrocortisone, early goal-directed therapy, insulin, and activated protein C in patients with severe sepsis and septic shock (hatched arrows). Abbreviation: WBC, white blood cell. American Journal of Kidney Diseases 2006 48, 838-841DOI: (10.1053/j.ajkd.2006.08.024) Copyright © 2006 National Kidney Foundation, Inc. Terms and Conditions