Recent observational results suggest that for patients with a rising BUN level and/or serum creatinine concentration, early consultation with a nephrologist can decrease the occurrence and mortality of ARF (10). The reasons for this observation are not clear but may involve early evaluation by the nephrologist of not only blood but also urinary chemistries, diminished incidence of fluid overload and need for mechanical ventilation, and perhaps earlier initiation of dialysis. On this background a search for sensitive parameters for the early diagnosis of ARF and a uniformly accepted definition of established ARF has emerged. A clinical definition of ARF has been sought that focuses on the degree of nitrogenous-waste accumulation in the blood, whether serum creatinine, BUN, or cystatin C (11), in order to make an early diagnosis. This approach, however, has important limitations. With established ARF the GFR is generally less than 10 ml/min. The amount of nitrogenous accumulation in the blood depends on the duration of the time that the patient has had a GFR of less than 10 ml/min. Thus, a catabolic patient with established ARF may have a serum creatinine concentration of 1.8 mg/dl when seen within the first 24 hours of established ARF, but the same individual may have a concentration of 10 mg/dl when seen after 5 days of established ARF, even though the GFR has been less than 10 ml/min in both circumstances. Nevertheless, acceptance of a 50% acute rise in serum creatinine to a concentration above 2.0 mg/dl as the clinical definition of ARF could increase the likelihood of early intervention and bring more consistency to the patient populations recruited for future intervention trials. However, such a definition does not differentiate among rises in serum creatinine that result (a) from a renal vasoconstriction–mediated prerenal azotemic state with intact tubular function, such as that which occurs with volume depletion, and advanced cardiac or liver failure; (b) from a postrenal azotemic state due to urinary tract obstruction; or (c) from established ARF due to an acute ischemic and/or nephrotoxic insult. A sensitive approach to ruling out postrenal azotemia is to identify post-void residual bladder urine as less than 50 ml and exclude pyelocalyceal dilatation using renal ultrasonography.