One of the most important functions of the kidney is the filtration and excretion of nitrogenous waste products from the blood. The measurements of elevated blood urea nitrogen (BUN) and creatinine serve as indicators of decreased renal function indicative of the decreased clearance of these waste products. AKI is currently defined as a rapid decline in the glomerular filtration rate (GFR) resulting in retention of nitrogenous wastes, primarily creatinine and blood urea nitrogen (542). Consequently, the diagnosis currently is dependent on the serial measurement over time of these substances in the blood of patients. The rapidity of this decline may occur over a time course of hours to months, but typically occurs over the course of hours to days. The ability of these measurements to serve as a surrogate marker of GFR is relatively imprecise (138, 363) and improved methods for evaluating GFR and a direct assessment of renal injury are sorely needed in the practice of medicine (96).
Clinically, AKI can be conveniently grouped into three primary etiologies: prerenal, renal, and postrenal (542). All three etiologies will be discussed briefly here; however, renal etiologies, especially those from ischemic and nephrotoxic injury, will receive the bulk of the discussion in this chapter given the frequency with which they occur and the fact that they are the etiologies associated with frank renal tissue injury.
Maintaining a normal GFR is dependent on adequate renal perfusion. Prerenal azotemia is characterized by a decrease in GFR due to a decrease in renal perfusion pressure without damage to the renal parenchyma (22). The kidneys receive up to 25% of the cardiac output and thus any failure of the general circulation or isolated failure of the intrarenal circulation can have a profound impact on renal perfusion. Causes of prerenal azotemia include: hypovolemia resulting from conditions such as hemorrh