Patients were excluded if they were younger than 15 years old, if they were on chronic dialysis or had a kidney transplant or if their length of hospital stay was shorter than 24 h. We screened all patients admitted to the Austin Hospital, Melbourne, Australia, between January 2000 and December 2002 using the computerized hospital admissions and discharges database. Therefore, we conducted a study using a large database of patients hospitalized in an academic medical center, concentrating on the meaning of BCR in patients with AKI. However, there is little evidence showing that BCR can distinguish between these two conditions and/or is clinically useful. The blood urea nitrogen (BUN)/creatinine ratio (BCR) is one of the common laboratory tests used to distinguish PRA and ATN, with a typical threshold of 20 (0.081 in international units) being suggested as a useful cut-off point for separating PRA from ATN. Furthermore, ATN has a much worse prognosis. Early recognition of the cause of AKI, especially distinguishing PRA and ATN, is widely considered clinically important as fluid resuscitation may improve PRA but can cause tissue edema and worsen ATN. These two causes have been reported to account for 66 to 75% of all cases of AKI. On the other hand, intra-renal diseases affect structures of the nephron such as the glomeruli, tubules, vessels or interstitium, and the most common cause of intra-renal (intrinsic) disease is thought to be acute tubular necrosis (ATN). Pre-renal failure, also called pre-renal azotemia (PRA), is described as a reversible increase in serum creatinine and urea concentrations resulting from decreased renal perfusion, which leads to a reduction in the glomerular filtration rate (GFR). The causes of AKI are often divided into three groups: pre-renal, intra-renal and post-renal. Acute kidney injury, acute tubular necrosis, blood urea nitrogen, creatinine, pre-renal azotemia IntroductionĪcute kidney injury (AKI) occurs commonly in hospitalized patients and carries a high mortality.
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