Manoeuvrier et al.

BMC Nephrology (2017) 18:173

DOI 10.1186/s12882-017-0591-9

RESEARCH ARTICLE Open Access

Diagnostic performance of serum blood

urea nitrogen to creatinine ratio for
distinguishing prerenal from intrinsic acute
kidney injury in the emergency department
Guillaume Manoeuvrier1, Kalyane Bach-Ngohou2, Eric Batard3,4, Damien Masson2 and David Trewick3,4*

Abstract
Background: The blood urea nitrogen to creatinine ratio (BCR) has been used since the early 1940s to help clinicians
differentiate between prerenal acute kidney injury (PR AKI) and intrinsic AKI (I AKI). This ratio is simple to use and often
put forward as a reliable diagnostic tool even though little scientific evidence supports this. The aim of this study was
to determine whether BCR is a reliable tool for distinguishing PR AKI from I AKI.
Methods: We conducted a retrospective observational study over a 13 months period, in the Emergency Department
(ED) of Nantes University Hospital. Eligible for inclusion were all adult patients consecutively admitted to the ED with a
creatinine >133 μmol/L (1.5 mg/dL).
Results: Sixty thousand one hundred sixty patients were consecutively admitted to the ED. 2756 patients had plasma
creatinine levels in excess of 133 μmol/L, 1653 were excluded, leaving 1103 patients for definitive inclusion.
Mean age was 75.7 ± 14.8 years old, 498 (45%) patients had PR AKI and 605 (55%) I AKI. BCR was 90.55 ± 39.32 and 91.
29 ± 39.79 in PR AKI and I AKI groups respectively. There was no statistical difference between mean BCR of the PR AKI
and I AKI groups, p = 0.758. The area under the ROC curve was 0.5 indicating that BCR had no capacity to discriminate
between PR AKI and I AKI.
Conclusions: Our study is the largest to investigate the diagnostic performance of BCR. BCR is not a reliable parameter
for distinguishing prerenal AKI from intrinsic AKI.
Keywords: Acute kidney injury (AKI), Blood urea creatinine ratio (BCR), Diagnostic performance, Emergency department,
Prerenal acute kidney injury

Background Under normal conditions, BCR is less than 100 (with

The blood urea nitrogen to creatinine ratio (BCR) has urea and creatinine concentrations expressed in mmol/
been used since the early 1940s to help clinicians diffe- L) [2–5]. In states of renal hypoperfusion with intact
rentiate between prerenal acute kidney injury (PR AKI) tubular function, blood urea nitrogen (BUN) is consi-
and intrinsic AKI (I AKI) [1]. This ratio is simple to use dered to rise out of proportion to plasma creatinine
and is often put forward as a reliable diagnostic tool. concentration, due to avid urea reabsorption by the
Indeed many textbooks of internal medicine, nephrology proximal tubule, the BCR typically becoming >100 [6].
and critical care continue to advocate the use of BCR One of the first to put forward this tool was Fishberg
even though its usefulness in the diagnosis and clinical in 1939 when he observed that “an increase in urea con-
management of AKI remains unclear [2–4]. tent of the blood may be considerable before the creati-
nine value rises in prerenal azotemia” [1]. However, as
* Correspondence: [email protected]
soon as 1947, other investigators found no such relation-
3
Department of Emergency Medicine, CHU Nantes, Nantes, France ship [7]. Since then, very few studies (human or animal)
4
Service des Urgences, CHU Hotel Dieu, 44000 Nantes, France have addressed the question and their results are
Full list of author information is available at the end of the article

© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
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(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Manoeuvrier et al. BMC Nephrology (2017) 18:173 Page 2 of 7

conflicting [8–11]. These studies consisted of small (Roche Diagnostics, Mannheim) according to the manu-
series of patients, essentially from intensive care units, facturer’s instructions.
the largest of which included only 103 patients and
this study was not specifically aimed at investigating Study definitions
BCR [11]. We defined AKI according to “Kidney Disease: Impro-
AKI is common in Emergency Departments (ED) ving Global Outcomes” (KDIGO) classification scheme
[12]. It can be challenging to differentiate prerenal from based on changes in plasma creatinine during the 7 days
intrinsic acute kidney injury in this setting. Indeed, the after admission (Table 1) [13]. Prerenal AKI (PR AKI)
ED physician has a short time frame to make decisions, was defined as non-obstructive AKI with a return of
he may not have access to current medication or base- plasma creatinine to 110% (or less) of baseline value
line creatinine, have incomplete medical history and during the 7 days following admission. The baseline
doesn’t have by definition the responsiveness to a fluid value of plasma creatinine was the lowest creatinine
challenge. measured 12 months before or after hospital admission.
The BCR is one of the diagnostic tools recommended Intrinsic AKI (I AKI) was defined as non-obstructive
to ED physicians for differentiating between PR and I AKI that didn’t meet the criteria of pre-renal AKI.
AKI, yet it has never been specifically studied in this
setting [3]. Chart review
The aim of this study was to determine whether BCR Patient’s records were reviewed using the hospital
is a reliable parameter for distinguishing prerenal from admissions and discharges database. Relevant data was
intrinsic AKI in a population of patients admitted to entered in a format that could be converted to an Excel
hospital via the ED. spreadsheet for analysis. The following information was
obtained for each admission: basic demographics, dates
Methods of hospital admission and discharge, admission plasma
Study design and patient selection creatinine, blood urea nitrogen (BUN) levels and BCR,
We conducted a retrospective observational study over a information concerning urinary obstruction, lowest
13 month period, from 1st of November 2013 to the creatinine measured 12 months before/after admission,
30th of November 2014, in the Medical Emergency lowest creatinine measured during the 7 days following
Department of Nantes University Hospital. Trauma pa- admission and presence or absence of AKI using KDIGO
tients were not admitted to this unit. The need for in- classification.
formed consent was waived by the institutional review
board of Nantes University Hospital because of the ano- Statistical analysis
nymous and purely observational nature of the study. All statistical analysis was performed using GraphPad
Eligible for inclusion were all adult patients (≥ 16 years Prism Software (La Jolla, CA, USA). Quantitative data
old) consecutively admitted to the ED with a creatinine were expressed as mean ± standard deviation (SD).
>133 μmol/L (1.5 mg/dL). Patients were excluded if on Comparison of biochemical and clinical data between
chronic dialysis or had a prior kidney transplant, stable prerenal AKI (PR AKI) and intrinsic AKI (I AKI)
chronic kidney disease, obstructive AKI, length of hos- patients was done using unpaired t-tests. Predictive
pital stay less than 48 h, no follow up creatinine during
the following 7 days of hospitalisation. If a patient was Table 1 Staging of Acute Kidney Injury (AKI) according to
admitted to the ED on several occasions during a 7 day KDIGO criteria
period, only the first creatinine >133 μmol/L was taken Stage Criteria
into account, the other admissions were excluded. Patients Stage 1 One of the following
with no baseline creatinine (lowest creatinine measured • Serum creatinine increased 1.5–1.9 times baseline
12 months before or after hospital admission) were • Serum creatinine increase >26.5 μmol/L (0.3 mg/dL)
also excluded. • Urinary output <0.5 mL/kg/h for 6–12 h
Stage 2 • Serum creatinine increase 2.0–2.9 times baseline
Laboratory techniques
Blood samples were collected and centrifuged at 2000 g • Urinary output <0.5 mL/kg/h for more than 12 h
for 10 min at 4 °C within 1 h after venipuncture. All bio- Stage 3 • Serum creatinine increase >3 times baseline
chemical measurements of urea and creatinine were per- • Serum creatinine increases to >353.6 μmol/L (4.0 mg/dL)
formed in the same laboratory (Laboratory of Clinical • Initiation of renal replacement therapy
Biochemistry, University Hospital of Nantes) respectively • Urinary output <0.3 mL/kg/h during more than 24 h
with an enzymatic kinetic UV assay and a kinetic colori-
• Anuria for more than 12 h
metric assay based on the Jaffé method on Cobas c701
Manoeuvrier et al. BMC Nephrology (2017) 18:173 Page 3 of 7

performance of BCR in terms of specificity and sensiti- (range [134–1089]; median 190) in the PR AKI and I AKI
vity was performed using Receiver Operating Characte- groups respectively (p = 0.002) (Fig. 2b and Table 2).
ristic (ROC) analysis. For all analyses, a P value <0.05 During the 7 days following admission, the patient’s
was considered to be statistically significant. lowest plasma creatinine concentrations were selected
and compared with their baseline creatinines (Fig. 2c
Results and Table 2). In the PR AKI group, the mean lowest
During the study period, 60,160 patients ≥16 years old creatinine concentrations during the 7 days follow-up
were consecutively admitted to the Emergency Department was 118.0 ± 65.2 μmol/L (range [30–606]; median 105).
of Nantes University Hospital. Creatinine levels were mea- The mean difference with plasma creatinine concentra-
sured 28,149 times for 26,299 patients. Two thousand tions at admission was 91.6 μmol/L. In the intrinsic AKI
seven hundred and fifty six had plasma creatinine levels in group, the mean lowest creatinine concentrations during
excess of 133 μmol/L but 1653 were excluded because they the 7 days follow-up was 162.4 ± 96.6 μmol/L (range
met one or more exclusion criteria, leaving 1103 patients [32–832]; median 138). The mean difference with
for definitive inclusion (Fig. 1). plasma creatinine concentrations at admission was
The demographic characteristics of the 1103 included 69.7 μmol/L. Mean difference between baseline and
patients are presented in Table 2. Mean age was lowest 7 day follow-up creatinine was significantly
75.7 ± 14.8 years old (range [16–103]; median 80), 693 lower in the PR AKI group than in I AKI group
(62.8%) were male. According to our definitions, 498 (p < 0.001) (Fig. 2c).
(45%) patients had prerenal AKI (PR AKI) and 605 The distribution of the blood urea nitrogen to creati-
(55%) intrinsic AKI (I AKI). The PR AKI and I AKI nine ratio (BCR) in the 2 groups is shown in Fig. 3. At
groups do not differ in terms of age (p = 0.518) admission, BCR was 90.6 ± 39.3 (range [24.4–262.7];
(Table 2). Patients are classified according to their median 83.0) and 91.3 ± 39.8 (range [9.8–269.1]; median
stage of AKI in Table 3. 81.8) in PR AKI and I AKI groups respectively. There
At admission, mean blood urea nitrogen (BUN) was no statistical difference between mean BCR of the
concentration was 18.1 ± 9.5 mmol/L (range [4.8–68.6]; prerenal AKI group and the intrinsic AKI group,
median 15.6) and 19.8 ± 9.6 mmol/L (range [4.0–68.7]; p = 0.758 (Fig. 3 and Table 2).
median 15.9) in PR AKI and I AKI groups respectively The prediction of the capacity of BCR to correctly
(p = 0.003) (Fig. 2a and Table 2). At admission, mean classify AKI as intrinsic or prerenal was further tested by
plasma creatinine concentration was 209.6 ± 118.3 μmol/L a Receiver Operating Characteristic (ROC) curve. The
(range [134–1376]; median 177) and 232.1 ± 124.8 μmol/L area under the curve was 0.5 indicating that the BCR

Fig. 1 Study Flow-chart – Patients admitted with plasma creatinine >133 μmol/L to the Medical Emergency Department of Nantes University
Hospital from 1st of November 2013 to the 30th of November 2014
Manoeuvrier et al. BMC Nephrology (2017) 18:173 Page 4 of 7

Table 2 Demographic and biological characteristics of patients with intrinsic AKI (I-AKI) and prerenal AKI (PR-AKI). Results are
presented as number of patients and proportions when appropriate or means (± standard deviation)
I-AKI PR-AKI P
(N = 605) (N = 498)
Age (years) 75.7 (14.3) 75.7 (15.3) 0.518
Gender, n male (%) 370 (61.2) 323 (64.9)
Plasma creatinine at admission (μmol/L) 232.1 (124.8) 209.6 (118.3) 0.002
Lowest plasma creatinine during the 7 days following admission (μmol/L) 162.4 (96.6) 118.0 (65.2) <0.001
Blood urea nitrogen at admission (mmol/L) 19.8 (9.6) 18.1 (9.5) 0.003
Blood urea nitrogen to creatinine ratio at admission (mmol/L/mmol/L) 91.3 (39.8) 90.6 (39.3) 0.758

had no capacity to discriminate between prerenal and in the real world. Indeed, many factors are known to
intrinsic AKI (Fig. 4). At the threshold of 100 commonly modify BCR independently of effective circulating vo-
used to distinguish PR AKI (BCR > 100) from I AKI lume. Gastro intestinal bleeding, a high protein diet, the
(BCR < 100), the sensitivity was 70.1% and the spe- catabolic effects of fever, trauma, infection, thyrotoxi-
cificity 32.6%. cosis, drugs such as tetracycline or corticosteroids, all in-
The distribution of patients with a BCR < 100 or >100 crease protein turnover resulting in increased hepatic
was further analysed and compared to renal recovery production of urea and increase BCR [5, 6]. Conversely,
(Table 4). in osmotic diuresis and with the use of acetazolamide,
If prerenal AKI was redefined as a return of serum proximal tubular reabsorption of salt and water is im-
creatinine to 110% of baseline in 72 h (rather than paired leading to an increase in excreted urea and a
7 days), 418 (38%) patients could be analysed. These are decrease in BCR even in states of hypovolemia. BCR also
the patients that had BUN and creatinine measured pre- decreases in patients with liver failure or protein malnu-
cisely at 72 h. Then 166 (39.7%) patients had PR AKI trition due to lower levels of BUN [5, 6]. One can also
and 252 (60.3%) I AKI. At admission, mean BCR was speculate that AKI is probably due to functional and in-
88.4 ± 39.6 (range [24.4–229.8]; median 82.8) and trinsic disease coexisting in different proportions, in a
95.3 ± 42.7 (range [9.8–269.1]; median 86.2) in PR AKI given patient at a given time. Indeed, it is assumed that
and I AKI groups respectively. There was no statistical a continuum exists which leads from prerenal to intrin-
difference between mean BCR of the prerenal AKI group sic AKI, the proportion of each changing over time [14].
and the intrinsic AKI group, p = 0.094. The area under It can then easily be assumed that BCR would only be
the ROC curve was 0.55. reliable if the underlying disease was 100% prerenal or
Analysis of patients presenting with acute heart failure 100% intrinsic, which is probably rarely the case.
(n = 191), typically associated with increased BCR, We chose a “cut off creatinine” for inclusion of patients
showed that 33% had PR AKI and 67% had I AKI, mean at 133 μmol/L. The reason for this was twofold: 1/ This
BCR was 98.3 ± 38 (range [37.3–250.6]; median 90.2). threshold is recognized as the highest creatinine level one
can have with a normal glomerular filtration rate (GFR) ie
Discussion 75 mL/min per 1.73m2 [15]. Indeed, a young (20–29 years
Our study is the largest concerning the diagnostic per- old) black male with a creatinine of 133 μmol/L would have
formance of BCR for differentiating prerenal from in- a normal GFR [15]. However, all creatinine levels above
trinsic AKI. It is the first to specifically investigate BCR 133 μmol/L are associated with altered GFRs. By including
in an unselected population of patients admitted to the only patients with creatinine levels greater than 133 μmol/L
Emergency Department. We have found that BCR had we were sure to only include patients with renal failure. 2/
no overall discriminative capacity in this setting, no mat- If we had included all 26,229 patients with a measured cre-
ter what threshold of BCR is chosen. atinine, we would have selected many healthy individuals
Even though the rationale underlying the use of BCR admitted to hospital for the first time. Many patients would
is seducing, our results show that it simply doesn’t work have met our exclusion criteria because of a short hospital
stay (< 48 h) and or no baseline creatinine.
Table 3 Staging of AKI patients according to KDIGO criteria A limitation that affects most studies on AKI, is the ab-
Stage 1 Stage 2 Stage 3 sence of a baseline creatinine for all patients. Indeed, the
Number of AKI patients (%) 334 (30.3) 576 (52.2) 193 (17.5) KDIGO classification scheme requires a baseline creatinine
PR AKI (%) 58.7 42.5 29.5
level to define AKI. In the absence of such values a method
of “imputation” or “back calculation” by reversing the
I AKI (%) 41.3 57.5 70.5
“Modification of Diet in Renal Disease” (MDRD) equation
Manoeuvrier et al. BMC Nephrology (2017) 18:173 Page 5 of 7

Fig. 3 Distribution of blood urea nitrogen to creatinine ratio (BCR)

according to AKI groups. The line in the middle of the box is plotted
at the median and whiskers delimit min to max values

using age, sex and an assumed normal GFR of 75 mL/min

per 1.73m2 has been recommended by the ADQI work-
group [16, 17]. This commonly accepted method underesti-
mates baseline creatinine and overestimates GFR [17, 18].
It has been shown that the incidence of AKI actually falls
when you rely excessively on the estimation of baseline
renal function by this method [12, 19]. Challinger et al.
found that 54% of the 745 patients included in their study
on AKI in the Emergency Department had no baseline
creatinine measurement. These patients were assumed to
have a normal estimated GFR. They found an overall inci-
dence of AKI of 24.4%, but this rose to 38.1% if only pa-
tients with known previous creatinine records were
included [12]. Because of this observation we decided to
exclude patients with no creatinine baseline (n = 255).
Our methodology induces 2 limitations. Firstly our
study was retrospective with the well-known limitations

Fig. 2 Distribution of blood urea nitrogen (BUN), plasma creatinine

values according to AKI groups. The box extends from the 25th to
75th percentiles. The line in the middle of the box is plotted at the
median and whiskers delimit min to max values. a - BUN values at
admission of patients with prerenal (PR AKI) and intrinsic AKI (I AKI);
(b) - Plasma creatinine values at admission of patients with PR AKI
and I AKI; (c) - Lowest plasma creatinine during the 7 days following
admission (Adm.) of patients with PR AKI and I AKI

Fig. 4 Receiver operating curve analysis of predictive performance

of blood urea nitrogen to creatinine ratio (BCR)
Manoeuvrier et al. BMC Nephrology (2017) 18:173 Page 6 of 7

Table 4 Distribution of prerenal and intrinsic AKI patients Abbreviations

according to whether BCR < or > 100 AKI: Acute kidney injury; BCR: Blood urea nitrogen to creatinine ratio;
BUN: Blood urea nitrogen; ED: Emergency department; GFR: Glomerular
BCR < 100 BCR > 100 filtration rate; I AKI: Intrinsic acute kidney injury; KDIGO: Kidney disease
Number of patients (%) 754 (68.4) 349 (31.6) improving global outcomes; MDRD: Modification of diet in renal disease;
N-GAL: Neutrophil gelatinase associated lipocalin; PR AKI: Prerenal acute
PR AKI (%) 45.9 43.6 kidney injury; ROC: Receiver operating characteristic
I AKI (%) 54.1 56.4
Acknowledgements
Not applicable.

of such studies and in particular it was not possible for Funding

us to assess the contribution of the “urine output”, No funding was obtained for this study.
component of the KDIGO criteria. Secondly there is no
Availability of data and materials
widely accepted definition of prerenal AKI [6]. The The datasets used and/or analysed during the current study are available
common observation is that it is a reversible condition, from the corresponding author on reasonable request.
but diagnostic criteria such as the amount, nature and
Authors’ contributions
duration of fluid resuscitation, time frame for reversibil- GM: Conception / design/ drafting. KB: Statistics, revising article. EB:
ity, or target creatinine improvement have not been ad- Conception, statistics, revising article. DM: Statistics, revising article. DT:
dressed. We defined prerenal AKI as a return of serum Conception/design/drafting/revising article. All authors have read and
approved the manuscript.
creatinine to 110% (or less) of the baseline value during
the 7 days following admission. In their review of AKI, Competing interests
Bagshaw et al. reported that time frames for defining The authors declare that they have no competing interests.

reversibility ie PR AKI, varied considerably from 48 h to Consent for publication

7 days or more and sometimes were not reported at all Not applicable.
[8]. The shorter (48-72 h) is the most published time
Ethics approval and consent to participate
frame but concerns almost exclusively patients from The need for informed consent was waived by the institutional review board
intensive care units, where blood samples are drawn of Nantes University Hospital because of the anonymous and purely
every day which is not necessarily the case for most observational nature of the study.

patients, such as ours, admitted to medical wards [6]. By

choosing a 72 h time frame for reversibility we would Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published
have had to exclude many patients who didn’t have maps and institutional affiliations.
blood samples precisely on day 3. We did however carry
out a subgroup analysis of these patients. We found 418 Author details
1
Department of Medicine, Clinique Jules Verne, Nantes, France. 2Department
(38%) patients that had BUN and creatinine measured at of Biology, Laboratory of Clinical Biochemistry, CHU Nantes, Nantes, France.
72 h. Again there was no statistical difference between 3
Department of Emergency Medicine, CHU Nantes, Nantes, France. 4Service
mean BCR of the prerenal and the intrinsic AKI groups, des Urgences, CHU Hotel Dieu, 44000 Nantes, France.
the area under the ROC curve was 0.55. Received: 1 February 2017 Accepted: 17 May 2017
Separating prerenal from intrinsic AKI remains cha-
llenging. No biological marker, whether old school (frac-
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