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The meaning of the blood urea nitrogen/creatinine ratio in acute kidney injury.

ABSTRACT: Background:A blood urea nitrogen (BUN)/creatinine ratio (BCR) >20 (0.081 in international unit) is used to distinguish pre-renal azotemia (PRA) and acute tubular necrosis (ATN). However, there is little evidence that BCR can distinguish between these two conditions and/or is clinically useful. Methods:We conducted a retrospective study using a large hospital database. Patients were divided into three groups: 'low BCR' (if BCR when acute kidney injury (AKI) developed was ?20), 'high BCR' (if BCR when AKI developed was >20) and 'no AKI' if patients did not satisfy any of the Risk, Injury, Failure, Loss and End-stage kidney disease criteria for AKI during hospitalization. Results:Among 20 126 study patients, 3641 (18.1%) had AKI. Among these patients, 1704 (46.8%) had a BCR <20 at AKI diagnosis ('low BCR') and 1937 (53.2%) had a BCR >20 ('high BCR'). The average BCR for the two groups was 15.8 versus 26.1 (P < 0.001). Hospital mortality was significantly less in the 'low-BCR' group (18.4 versus 29.9%, P < 0.001). Multivariable logistic regression analysis for hospital mortality ('no AKI' as a reference) showed that the odds ratio of 'high BCR' (5.73) was higher than that of 'low BCR' (3.32). Conclusions:Approximately half of the patients with AKI have a BCR >20, the traditional threshold of diagnosing PRA. Unlike PRA patients who have a lower mortality than ATN patients, high BCR patients had higher hospital mortality compared with low BCR patients, which was confirmed with multivariable analysis. These findings do not support BCR as a marker of PRA.

SUBMITTER: Uchino S

PROVIDER: S-EPMC5783213 | biostudies-literature | 2012 Apr

REPOSITORIES: biostudies-literature

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The meaning of the blood urea nitrogen/creatinine ratio in acute kidney injury.

Uchino Shigehiko S Bellomo Rinaldo R Goldsmith Donna D

Clinical kidney journal 20120401 2

<h4>Background</h4>A blood urea nitrogen (BUN)/creatinine ratio (BCR) >20 (0.081 in international unit) is used to distinguish pre-renal azotemia (PRA) and acute tubular necrosis (ATN). However, there is little evidence that BCR can distinguish between these two conditions and/or is clinically useful.<h4>Methods</h4>We conducted a retrospective study using a large hospital database. Patients were divided into three groups: 'low BCR' (if BCR when acute kidney injury (AKI) developed was ≤20), 'hig ...[more]

PMID: 29497527

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Project description:The diagnosis of acute kidney injury (AKI), which is currently defined as an increase in serum creatinine (Scr) concentration, provides little information on the condition's actual cause. To improve phenotyping of AKI, many urinary biomarkers of tubular injury are being investigated. Because AKI cases are not frequently biopsied, the diagnostic accuracy of concentrations of Scr and urinary biomarkers for histologic acute tubular injury is unknown.Cross-sectional analysis from multicenter prospective cohort.Hospitalized deceased kidney donors on whom kidney biopsies were performed at the time of organ procurement for histologic evaluation.(1) AKI diagnosed by change in Scr concentration during donor hospitalization and (2) concentrations of urinary biomarkers (neutrophil gelatinase-associated lipocalin [NGAL], liver-type fatty acid-binding protein [L-FABP], interleukin 18 [IL-18], and kidney injury molecule 1 [KIM-1]) measured at organ procurement.Histologic acute tubular injury.Of 581 donors, 98 (17%) had mild acute tubular injury and 57 (10%) had severe acute tubular injury. Overall, Scr-based AKI had poor diagnostic performance for identifying histologic acute tubular injury and 49% of donors with severe acute tubular injury did not have AKI. The area under the receiver operating characteristic curve (AUROC) of change in Scr concentration for diagnosing severe acute tubular injury was 0.58 (95% CI, 0.49-0.67) and for any acute tubular injury was 0.52 (95% CI, 0.45-0.58). Compared with Scr concentration, NGAL concentration demonstrated higher AUROC for diagnosing both severe acute tubular injury (0.67; 95% CI, 0.60-0.74; P=0.03) and any acute tubular injury (0.60; 95% CI, 0.55-0.66; P=0.005). In donors who did not have Scr-based AKI, NGAL concentrations were higher with increasing severities of acute tubular injury (subclinical AKI). However, compared with Scr concentration, AUROCs for acute tubular injury diagnosis were not significantly higher for urinary L-FABP, IL-18, or KIM-1.The spectrum of AKI cause in deceased donors may be different from that of a general hospitalized population.Concentrations of Scr and kidney injury biomarkers (L-FABP, IL-18, and KIM-1) lack accuracy for diagnosing acute tubular injury in hospitalized deceased donors. Although urinary NGAL concentration had slightly higher discrimination for acute tubular injury than did Scr concentration, its overall AUROC was still modest.

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The meaning of the blood urea nitrogen/creatinine ratio in acute kidney injury.

Publications

The meaning of the blood urea nitrogen/creatinine ratio in acute kidney injury.

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