Renal vascular resistance in sepsis.
OBJECTIVE
To assess changes in renal vascular resistance (RVR) in human and experimental sepsis and to identify determinants of RVR.


METHODS
We performed a systematic interrogation of two electronic reference libraries using specific search terms. Subjects were animals and patients involved in experimental and human studies of sepsis and septic acute renal failure, in which the RVR was assessed. We obtained all human and experimental articles reporting RVR during sepsis. We assessed the role of various factors that might influence the RVR during sepsis using statistical methods.


RESULTS
We found no human studies, in which the renal blood flow (and, therefore, the RVR) was measured with suitably accurate direct methods. Of the 137 animal studies identified, 52 reported a decreased RVR, 16 studies reported no change in RVR, and 69 studies reported an increased RVR. Consciousness of animals, duration of measurement, method of induction of sepsis, and fluid administration had no effect on the RVR. On the other hand, on univariate analysis, size of the animals (p < 0.001), technique of measurement (p = 0.017), recovery after surgery (p = 0.004), and cardiac output (p < 0.001) influenced the RVR. Multivariate analysis, however, showed that only cardiac output (p = 0.028) and size of the animals (p = 0.031) remained independent determinants of the RVR.


CONCLUSIONS
Changes in RVR during sepsis in humans are unknown. In experimental sepsis, several factors not directly related to sepsis per se appear to influence the RVR. A high cardiac output and the use of large animals predict a decreased RVR, while a decreased cardiac output and the use of small animals predict an increased RVR.
Langenberg
Christoph
C
Departments of Intensive Care and Medicine, Austin Hospital and University of Melbourne, Heidelberg, Melbourne, Australia.
Bellomo
Rinaldo
R
May
Clive N
CN
Egi
Moritoki
M
Wan
Li
L
Morgera
Stanislao
S
D058186:Acute Kidney Injury / Q000209:etiology / Q000503:physiopathology*; D000818:Animals; D049628:Body Size; D002302:Cardiac Output; D006801:Humans; D007668:Kidney / Q000098:blood supply* / Q000503:physiopathology; D023421:Models, Animal; D012079:Renal Circulation; D018805:Sepsis / Q000150:complications / Q000503:physiopathology*; D014655:Vascular Resistance; D014661:Vasoconstriction