title: Renal blood flow in sepsis.
abstract: BACKGROUND
  To assess changes in renal blood flow (RBF) in human and experimental sepsis, and to identify determinants of RBF.
  
  
  METHODS
  Using specific search terms we systematically interrogated two electronic reference libraries to identify experimental and human studies of sepsis and septic acute renal failure in which RBF was measured. In the retrieved studies, we assessed the influence of various factors on RBF during sepsis using statistical methods.
  
  
  RESULTS
  We found no human studies in which RBF was measured with suitably accurate direct methods. Where it was measured in humans with sepsis, however, RBF was increased compared with normal. Of the 159 animal studies identified, 99 reported decreased RBF and 60 reported unchanged or increased RBF. The size of animal, technique of measurement, duration of measurement, method of induction of sepsis, and fluid administration had no effect on RBF. In contrast, on univariate analysis, state of consciousness of animals (P = 0.005), recovery after surgery (P < 0.001), haemodynamic pattern (hypodynamic or hyperdynamic state; P < 0.001) and cardiac output (P < 0.001) influenced RBF. However, multivariate analysis showed that only cardiac output remained an independent determinant of RBF (P < 0.001).
  
  
  CONCLUSIONS
  The impact of sepsis on RBF in humans is unknown. In experimental sepsis, RBF was reported to be decreased in two-thirds of studies (62 %) and unchanged or increased in one-third (38%). On univariate analysis, several factors not directly related to sepsis appear to influence RBF. However, multivariate analysis suggests that cardiac output has a dominant effect on RBF during sepsis, such that, in the presence of a decreased cardiac output, RBF is typically decreased, whereas in the presence of a preserved or increased cardiac output RBF is typically maintained or increased.
authors.affiliation: Department of Intensive Care, Austin Hospital, and University of Melbourne, Heidelberg, Melbourne, Australia.
authors.forename: Christoph
authors.initials: C
authors.lastname: Langenberg
authors.forename: Rinaldo
authors.initials: R
authors.lastname: Bellomo
authors.forename: Clive
authors.initials: C
authors.lastname: May
authors.forename: Li
authors.initials: L
authors.lastname: Wan
authors.forename: Moritoki
authors.initials: M
authors.lastname: Egi
authors.forename: Stanislao
authors.initials: S
authors.lastname: Morgera
mesh_terms: D000818:Animals; D002302:Cardiac Output; D004195:Disease Models, Animal; D006439:Hemodynamics; D006801:Humans; D008954:Models, Biological; D012079:Renal Circulation; D018805:Sepsis / Q000503:physiopathology*