The kidney, one of the most injured organs in critically ill patients, is faced with unique challenges for molecular oxygen regulation. Recent research activities in the pathophysiological mechanism of acute renal injury (ARI) emphasize the central role of hemodynamic and inflammatory events in septic shock. More particularly, two mechanisms have been postulated to explain the inability of the injured kidney to extract oxygen: tissue hypoxia and cellular energetic metabolism dysfunction. The present investigation was carried out to characterize the effects of bacterial endotoxin on the oxygen consumption of human tubular proximal cell line (PTC) by using the very sensitive electron spin resonance oximetry method. Oxygen consumption was shown to decrease quite markedly in cells treated with lipopolysaccharide (LPS) from 16.52 ± 2.51 (n=6) in the control group to: 12.94 ± 2.62 (n=3) in the short incubation time group (6h) and 10.86 ± 2.20 (n=3) in the long incubation time group (18h). This decrease in oxygen consumption in renal cells after LPS challenge may be in relation with a metabolic down-regulation. Renal energetic are deranged in sepsis not just because O2 delivery is impaired but perhaps also because the ability of cells to utilize available O2 is compromised.