Acute renal failure (ARF) is a common condition on the intensive care unit (ICU) and may affect up to 40% of patients (de Mendonca, A. et al., 2000), (Korkeila, M. et al., 2000). Pathophysiological mechanisms remain unclear. Patients who die from sepsis have kidneys that look histologically normal (Hotchkiss, R.S. et al., 1999), while the renal prognosis in survivors is good with < 2% requiring long-term renal replacement therapy (Noble, J.S. et al., 2001). This has led some authors to suggest that acute renal failure is a physiological process designed to shut down vital processes and protect the kidney from irreversible damage during a severe insult (Singer, M. et al., 2004). As ninety percent of oxygen consumption is utilised by the mitochondrion (Babcock, G.T. and Wikstrom, M., 1992), metabolic control may be regulated by mitochondrial activity (Beltran, B. et al., 2000). This may be an important mechanism underlying renal failure but is difficult to assess in the intact animal.