Based on the foregoing comments, this discussion of mechanisms of ARF will not include nitrogenous-waste accumulation due to renal vasoconstriction with intact tubular function (prerenal azotemia) or urinary tract obstruction (postrenal azotemia). The mechanisms of ARF involve both vascular and tubular factors (15). An ischemic insult to the kidney will in general be the cause of the ARF discussed herein. While a decrease in renal blood flow with diminished oxygen and substrate delivery to the tubule cells is an important ischemic factor, it must be remembered that a relative increase in oxygen demand by the tubule is also a factor in renal ischemia.
The term ATN, although frequently used to describe the syndrome of clinical ARF in the absence of prerenal and postrenal azotemia, is somewhat of a misnomer. Specifically, in established ARF the presence of tubular necrosis upon histological examination of the kidney is seen in only occasional tubule cells at best and, in some cases, may not even be detectable (16). What is clear with established ARF, however, is that the glomeruli are morphologically normal. This perhaps justifies the investigative focus on renal tubules. The following discussion will describe some of the vascular, tubular, and inflammatory perturbations that occur with an acute renal insult. An attempt will then be made to integrate the important underlying pathogenetic factors.