The differentiation of prerenal azotemia and established ARF, however, has proven more difficult. Several biomarkers have been proposed for the early diagnosis of ARF and are currently under study. These include increased urinary excretion of kidney injury molecule-1 (12), IL-18 (13), and tubular enzymes (14). In order for any of these or other potential future biomarkers to become practical in the early clinical diagnosis of established ARF, specificity, sensitivity, rapid availability, cost effectiveness, and advantages as compared with the inexpensive and readily available measure of FENa must be considered.
From a clinical-diagnostic viewpoint, a potential advancement may be an agreement to use the term ARF, rather than ATN, independent of whether the acute insult was ischemic or nephrotoxic. Such an agreement, however, would also necessitate using the terms prerenal azotemia and postrenal azotemia for those potentially reversible conditions that result from renal vasoconstriction and urinary tract obstruction, respectively. Alternatively, it must be recognized that diagnosis of ARF based solely on a given rise in serum creatinine, BUN, or cystatin C levels would encompass many patients who do not have the clinical syndrome of established ARF, an entity that is not readily reversible by fluid resuscitation, cardiac or hepatic functional improvement, or relief of a urinary tract obstruction.