There is no question that renal tubule dysfunction occurs in established ARF, since tubular sodium reabsorption is decreased, i.e., FENa > 2.0, at a time when normal renal tubules avidly increase tubular sodium reabsorption in response to renal vasoconstriction. However, investigators of tubular abnormalities, which occur following acute renal ischemic insults, must ultimately demonstrate how the observed tubule perturbation mediates the fall in GFR to less than 10% of normal — the hallmark of established ARF.