Hindawi

International Journal of Nephrology

Volume 2017, Article ID 5241482, 8 pages
https://doi.org/10.1155/2017/5241482

Research Article
Incidence and Risk Factors for Early Acute
Kidney Injury in Nonsurgical Patients: A Cohort Study

Javier Enrique Cely,1,2 Elkin José Mendoza,1,2

Carlos Roberto Olivares,2 Oscar Julián Sepúlveda,1 Juan Sebastián Acosta,1
Rafael Andrés Barón,1 and Juan José Diaztagle1,3
1
Department of Internal Medicine, Fundación Universitaria de Ciencias de la Salud, San Jose Hospital,
School of Medicine, Bogotá, Colombia
2
Department of Nephrology, Dialysis and Transplantation, Fundación Universitaria de Ciencias de la Salud,
San Jose Hospital, School of Medicine, Bogotá, Colombia
3
Department of Physiological Sciences, School of Medicine, Universidad Nacional de Colombia, Bogota branch, Bogotá, Colombia

Correspondence should be addressed to Javier Enrique Cely; javiercelynsd@hotmail.com

Received 27 November 2016; Revised 14 March 2017; Accepted 28 March 2017; Published 11 April 2017

Academic Editor: Ziyad Al-Aly

Copyright © 2017 Javier Enrique Cely et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.

Introduction. Detecting acute kidney injury (AKI) in the first days of hospitalization could prevent potentially fatal complications.
However, epidemiological data are scarce, especially on nonsurgical patients. Objectives. To determine the incidence and risk factors
associated with AKI within five days of hospitalization (EAKI). Methods. Prospective cohort of patients hospitalized in the Internal
Medicine Department. Results. A total of 16% of 400 patients developed EAKI. The associated risk factors were prehospital treatment
with nephrotoxic drugs (2.21 OR; 95% CI 1.12–4.36, 𝑝 = 0.022), chronic kidney disease (CKD) in stages 3 to 5 (3.56 OR; 95% CI
1.55–8.18, 𝑝 < 0.003), and venous thromboembolism (VTE) at admission (5.05 OR; 95% CI 1.59–16.0, 𝑝 < 0.006). The median
length of hospital stay was higher among patients who developed EAKI (8 [IQR 5–14] versus 6 [IQR 4–10], 𝑝 = 0.008) and was
associated with an increased requirement for dialysis (4.87 OR 95% CI 2.54 to 8.97, 𝑝 < 0.001) and in-hospital death (3.45 OR; 95%
CI 2.18 to 5.48, 𝑝 < 0.001). Conclusions. The incidence of EAKI in nonsurgical patients is similar to the worldwide incidence of
AKI. The risk factors included CKD from stage 3 onwards, prehospital treatment with nephrotoxic drugs, and VTE at admission.
EAKI is associated with prolonged hospital stay, increased mortality rate, and dialysis requirement.

1. Introduction The mission of healthcare institutions is to know local

epidemiology and to generate prevention strategies based on
Acute kidney injury (AKI) has a high impact on healthcare
the knowledge of risk factors, which should be identified early
systems because of its high morbidity and mortality rates,
length of hospital stay, and treatment costs [1–3]. Thus, pre- upon hospital admission, towards eradicating in-hospital
vention and early diagnosis are essential to provide measures preventable deaths from AKI [7]. Such factors have already
to avoid the onset of dialysis as much as possible. Although been reported in previous publications and are best known
molecular markers of early kidney damage would be ideal [4], in the septic population and within intensive (ICU) and post-
they are, unfortunately, unavailable for routine clinical use. operative (PCU) care units, among others [8–10]. Specifically,
Therefore, variations in serum creatinine according to the conditions such as diabetes, proteinuria, and reduced renal
Acute Kidney Injury Network (AKIN) and Kidney Disease function on admission have been reportedly linked to the
Improve Global Outcome (KDIGO) criteria remain a valid development of AKI in patients with severe sepsis [11]. How-
tool for diagnosis [5, 6]. ever, we do not know whether these criteria apply to other
2 International Journal of Nephrology

scenarios, including nonsurgical patients and during early direct patient examination. A project coordinator was
hospitalization. responsible for conducting the daily patient census and as-
To date, there have been no identifiable studies that sessing the eligibility criteria and monitoring. In case of
evaluate variables related to the development of EAKI in doubt, a medical research group formed by three nephrolo-
this subset of nonsurgical patients who are managed by an gists (evaluation group) performed the final patient classifi-
Internal Medicine team. The importance of these studies lies cation.
in providing a useful tool for clinicians to prevent the pro-
gression of the disease and to help avoid morbid treatments 2.3. Variables. Clinically relevant variables included history
such as dialysis. Therefore, the present study aims to assess the of AHT, DM, heart failure, cirrhosis, coronary heart dis-
incidence and risk factors associated with the development ease, rheumatologic disease, nephrotic syndrome, and CKD.
of AKI in nonsurgical patients, including a population with According to the National Kidney Foundation Kidney Dis-
CKD and at early stages of hospitalization. ease Outcomes Quality Initiative (NKF KDOQI) guideline,
CKD was defined as GFR ≥ 60 mL/min/1.73 m2 with structur-
2. Materials and Methods al or functional kidney abnormality (abnormal composition
of urine and/or abnormal imaging studies) for ≥3 months or
2.1. Study Design and Patients. A prospective cohort study GFR < 60 mL/min/1.73 m2 with or without kidney damage for
was performed at the San Jose Hospital in Bogota Colombia, a ≥3 months [12]. Similarly, CKD was staged from 1 to 5
level-four university hospital that provides healthcare to more according to the NFK-KDOQI guideline with the GFR
than 2,500 patients per year in the Internal Medicine Depart- estimated by the CKD-EPI equation using the creatinine on
ment and has a Nephrology and Dialysis Department and admission [13]. Stages 1 and 2 were analyzed as a single varia-
a transplantation unit. We included adult patients admitted ble and stages 3, 4, and 5 as another variable for two reasons:
for emergency care and hospitalized in the Internal Medicine first, the number of patients with CKD in stages 1, 4, and 5
Department for more than 48 hours from September 2015 to was poor in the cohort and, secondly, the risk of AKI in pa-
April 2016. Patients on chronic dialysis or meeting the criteria tients with reduced GFR from 60 mL/min/1.73 m2 (stages 3, 4,
for urgent dialysis on admission, pregnant, of history of and 5) is better known in previous publications; however, it is
kidney transplantation, of community-acquired acute kidney uncertain for stages 1 and 2 (GFR ≥ 60 mL/min/1.73 m2 with
injury (CA-AKI), or transferred to the ICU within 48 hours structural or functional kidney abnormality) [14].
were excluded from the study. Creatinine levels were mea- Other variables of interest assessed included age, sep-
sured on admission, at 48 hours and on day 5 of hospital sis, hydration status on admission based on the attending
stay, to establish the presence of AKI, based on the following physician’s criteria, main diagnosis on admission, prehospital
operational definitions. and in-hospital treatment with nephrotoxic drugs shown in
Table 1 (the operational definitions for nephrotoxic drugs are
EAKI. Patient admitted with normal creatinine levels (the
shown in Table 1 of Supplementary Material available online
creatinine reference values were used according to the local
at https://doi.org/10.1155/2017/5241482), ICU admission after
clinical laboratory men ≤ 1.3 mg/dL and women ≤ 1.1 mg/dL)
48 hours of hospital stay, dialysis requirement, length of hos-
and with an increase in creatinine equal to or greater than 0.3
pital stay (including days of ICU stay if admitted 48 hours
mg/dL when comparing creatinine on admission with the
after hospital admission), and in-hospital death.
control at 48 hours or on day five (based on the diagnostic
recommendations of the KDIGO guidelines for AKI, the
criterion based on changes in urinary output was not consid- 2.4. Sample Size. Sample size calculation was performed
ered) [6]. using a logistic regression model based on a prevalence of
hospital-acquired AKI of approximately 17.2% [15, 16] and
CA-AKI. Patients with increased creatinine on admission and expecting to obtain at least 10 events for each of the five
some of the following conditions: covariates considered to be the most important risk factors:
CKD at admission, administration of nephrotoxic drugs, age,
(i) An increase ≥0.3 mg/dL creatinine on admission
history of diabetes mellitus (DM), and sepsis [10, 11, 14]. The
compared with a prehospital record of creatinine six
result is a minimum required sample size of 348 patients.
months before admission
(ii) If no previous record exists, the evaluation group was
2.5. Statistical Methods. A database was constructed and
responsible for the clinical and paraclinical assess-
statistical analysis was performed using STATA 13. Descrip-
ment (i.e., renal diagnostic imaging, abnormal bone
tive statistics were used to report the absolute and relative
mineral metabolism, or other findings suggestive of
frequencies of categorical variables, and measures of central
CKD) to define CA-AKI or CKD without AKI
tendency and dispersion were used for quantitative variables,
(iii) Creatinine levels at the end of hospitalization lower considering their distribution based on the Shapiro-Wilk test.
than the creatinine levels on admission with a differ- The Mann–Whitney 𝑈 test was used for quantitative variables
ence ≥0.3 mg/dL with abnormal distribution. The incidence of EAKI was cal-
culated.
2.2. Source and Monitoring Methods. Data were collected A bivariate analysis was performed to assess the relation-
from electronic medical records and were corroborated by ship between independent variables (exposure) and EAKI
International Journal of Nephrology 3

Table 1: Population characteristics.

Variable Total Early acute kidney injury

𝑝 value
𝑛 (%) or median (IQR) 𝑛 = 400 No (𝑛 = 336) Yes (𝑛 = 64)
Age (years) 65 (49–77) 64 (47–77) 68 (58–81) 0.033
Sex (male) 180 (45) 151 (44.9) 29 (45.3) 0.776
Weight (kg) 64.4 (54.9–75) 64.1 (55–75) 66 (54.4–74.1) 0.993
Anemia 138 (34.5) 111 (33.0) 27 (42.19) 0.158
History of diabetes mellitus 91 (22.7) 69 (20.5) 22 (34.4) 0.015
History of AHT 194 (48.5) 155 (46.1) 39 (60.9) 0.030
History of cirrhosis 10 (2.5) 8 (2.4) 2 (3.13) 0.727
History of heart failure 71 (17.7) 57 (16.9) 14 (21.8) 0.346
History of coronary heart disease 44 (11) 34 (10.1) 10 (15.6) 0.197
History of rheumatologic disease 40 (10) 36 (10.7) 4 (6.3) 0.275
CKD∗ at admission 243 (60.7) 149 (44.3) 19 (29.7)
Stage 1 (>90 mL/min/1.73 m2 ) 6 (1.5) 6 (1.5) 0 (0)
Stage 2 (60–90 mL/min/1.73 m2 ) 162 (40.5) 143 (42.6) 19 (29.7)
<0.001
Stage 3 (30–59 mL/min/1.73 m2 ) 65 (16.2) 46 (13.7) 19 (29.7)
Stage 4 (15–29 mL/min/1.73 m2 ) 6 (1.5) 1 (0.3) 5 (7.8)
Stage 5 (<15 mL/min/1.73 m2 ) 4 (1) 2 (0.6) 2 (13.1)
In-hospital treatment with nephrotoxic drugs 376 (94) 315 (93.7) 61 (95.3)
Contrast 81 (20.2) 68 (20.2) 13 (20.3)
NSAIDs 44 (11) 40 (11.9) 4 (6.3)
Vancomycin 17 (4.2) 14 (4.2) 3 (4.7)
Proton pump inhibitor 314 (78.5) 264 (78.6) 50 (78.1)
Quinolones 2 (0.5) 2 (0.6) 0 (0)
0.630
Aminoglycosides 1 (0.25) 0 (0) 1 (1.6)
Polymyxin B 1 (0.25) 1 (0.3) 0 (0)
IECA/ARAII 168 (42) 139 (41.4) 29 (45.3)
Furosemide 125(31.2) 95 (28.3) 30 (46.9)
Potassium-sparing diuretics 32 (8) 26 (7.7) 6 (9.4)
Thiazide diuretics 12 (3) 11 (3.3) 1 (1.6)
Prehospital treatment with potentially nephrotoxic drugs 239 (59.7) 190 (56.5) 49 (76.6)
Statins 70 (17.5) 61 (18.2) 9 (14.6)
NSAIDs 54 (13.5) 44 (13.1) 10 (15.6)
Quinolones 1 (0.25) 1 (0.3) 0 (0)
Aminoglycosides 1 (0.25) 0 (0) 1 (1.6) 0.003
IECA/ARAII 172 (43) 140 (41.7) 32 (50.0)
Furosemide 84 (21) 62 (18.5) 22 (34.4)
Potassium-sparing diuretics 33 (8.25) 28 (8.3) 5 (7.8)
Thiazide diuretics 33 (8.25) 25 (7.4) 8 (12.5)
Primary diagnosis on admission
Bacterial infection 172 (43) 149 (44.4) 23 (35.9)
Cardiovascular disease 75 (18.7) 58 (17.3) 17 (26.6)
Chronic pulmonary and pleural disease 59 (14.7) 53 (15.8) 6 (9.4) <0.001
Endocrine disease 18 (4.5) 12 (3.6) 6 (9.4)
Venous thromboembolism 19 (4.7) 13 (3.9) 6 (9.4)
Others† 57 (14.2) 51 (15.2) 6 (9.4)
Hydrated 119 (29.7) 104 (30.9) 15 (23.4) 0.228
Sepsis‡ 159 (39.7) 137 (40.8) 22 (34.4) 0.338
Nephrotic syndrome 4 (1) 2 (0.6) 2 (3.1) 0.062
Isolated proteinuria 51 (12.7) 40 (11.9) 11 (17.2) 0.246
Days of hospital stay 7 (4–11) 6 (4–10) 8 (5–14) 0.009
ICU requirement 34 (8.5) 25 (7.4) 9 (14.1) 0.082
4 International Journal of Nephrology

Table 1: Continued.
Variable Total Early acute kidney injury
𝑝 value
𝑛 (%) or median (IQR) 𝑛 = 400 No (𝑛 = 336) Yes (𝑛 = 64)
Renal replacement therapy 4 (1) 1 (0.3) 3 (4.7) <0.001
Condition on discharge (death) 30 (7.5) 16 (4.8) 14 (21.9) <0.001
∗
Calculated using the chronic kidney disease epidemiology collaboration (CKD-EPI) equation and classified based on NFK-KDOQI guideline.
†
Including gastrointestinal disease, rheumatologic disease, glomerular and tubulointerstitial disease, nonneoplastic hematologic disease, solid tumors and
hematological malignancies, and viral infections.
‡
Defined as systemic inflammatory response syndrome (SIRS) with septic focus.

Screened patients
n = 1208
(i) 239 CA-AKI
(ii) 198 management by another specialty
or ICU requirements within 48 h
Excluded patients (iii) 142 discharge or death within 48 h
n = 808 (iv) 106 dialysis therapy or kidney
transplantation
(v) 47 referral from another institution
Cohort (vi) 38 readmission within 7 days
n = 400 (100%) (vii) 15 emergency dialysis
(viii) 23 others

EAKI
n = 64 (16%)

Without EAKI
n = 336 (84%)

Figure 1: Cohort selection process.

using the Chi-squared (𝜒2 ) test. Subsequently, a multivariate admission were 0.9 mg/dL (IQR 0.7–1). The most common
analysis by logistic regression model with odds ratio (OR) cal- diagnosis on admission was bacterial infection and the most
culation was done. All clinically relevant variables and those common comorbidity was AHT followed by DM (Table 1).
with 𝑝 values < 0.1 were included in the analysis. A 𝑝 value Some 16% (𝑛 = 64) of the population developed EAKI,
< 0.05 was considered significant in the multivariate analysis. classified as 84.4% KDIGO 1 (𝑛 = 54), 12.5% KDIGO 2
Variables without relevance to the model were removed using (𝑛 = 8), and 3.1% KDIGO 3 (𝑛 = 2), depending on the severity
a backward strategy. The goodness of fit was based on Hosmer of renal injury [6].
and Lemeshow criteria. The following variables were associated with the develop-
ment of EAKI in the bivariate analysis. Age (OR 1.02; 95% CI
2.6. Ethics. Ethical principles of the Declaration of Helsinki
1.00 to 1.03, 𝑝 = 0.019), CKD on admission stages 3, 4, and
and Colombian regulations issued by the Ministry of Health
5 (OR 4.00; 95% CI 2.13 to 7.45 𝑝 < 0.001), history of DM
pursuant to resolution 8430 of 1993 were considered. The
(OR 2.06; 95% CI 1.09 to 3.80), history of AHT (OR 1.82; 95%
protocol was approved by the Research Committee of the
CI 1.02 to 3.28, 𝑝 = 0.030), and prehospital treatment with
School of Medicine of the Foundation University of Health
Sciences and the Ethics Committee on Human Research of nephrotoxic drugs (OR 2.63; 95% CI 1.38 to 5.25, 𝑝 = 0.002)
San Jose Hospital, Bogotá. (Table 2). The individual analysis of each nephrotoxic drug
revealed that prehospital (OR 2.31; 95% CI 1.22 to 4.30, 𝑝 =
0.004) or in-hospital (OR 2.24; 95% CI 1.24 to 4.00, 𝑝 = 0.003)
3. Results
treatment with furosemide was associated with EAKI.
A total of 1,208 patients were evaluated during the collection In the logistic regression EAKI was associated with CKD
period, including 400 who met the inclusion criteria (Fig- on admission stages 3, 4, and 5 (OR 3.56; 95% CI 1.55 to
ure 1). A total of 55% (𝑛 = 220) were women, the median age 8.18, 𝑝 = 0.003), prehospital treatment with nephrotoxic
was 65 years (IQR 49–77), and the median creatinine levels on drugs (OR 2.21; 95% CI 1.12 to 4.36, 𝑝 = 0.022), and venous
International Journal of Nephrology 5

Table 2: Risk factors associated with EAKI, bivariate analysis.

Variable OR 95% CI 𝑝 value
CKD∗ stages 1 and 2 0.93 [0.44–1.93] 0.824
CKD∗ stages 3, 4, and 5 4.00 [2.13–7.45] <0.001
Prehospital treatment with nephrotoxic drugs 2.63 [1.38–5.25] 0.002
In-hospital treatment with nephrotoxic drugs 1.35 [0.39–7.31] 0.630
Contrast media 1.00 [0.47–2.00] 0.990
History of DM 2.06 [1.09–3.80] 0.013
History of AHT 1.82 [1.02–3.28] 0.030
History of cirrhosis 1.32 [0.13–6.84] 0.730
History of heart failure 1.37 [0.65–2.73] 0.350
History of rheumatologic disease 0.55 [0.14–1.64] 0.260
History of coronary heart disease 1.64 [0.68–3.65] 0.197
Nephrotic syndrome 5.39 [0.38–75.1] 0.062
Age 1.02 [1.00–1.03] 0.019
Hydration status 0.68 [0.34–1.30] 0.230
Sepsis 0.38 [0.76–1.37] 0.338
Venous thromboembolism at admission 2.57 [0.77–7.59] 0.057
Cardiovascular disease at admission 1.73 [0.87–3.33] 0.086
Chronic pulmonary and pleural disease at admission 0.55 [0.18–1.37] 0.185
∗
Calculated using the chronic kidney disease epidemiology collaboration (CKD-EPI) equation and classified based on NFK-KDOQI guidelines.

Table 3: Risk factors associated with EAKI, multivariate analysis.

Variable OR 95% CI 𝑝 value
CKD∗ stages 1 and 2 0.83 [0.39–1.75] 0.628
CKD∗ stages 3, 4 and 5 3.56 [1.55–8.18] 0.003
Prehospital treatment with nephrotoxic drugs 2.21 [1.12–4.36] 0.022
Venous thromboembolism at admission 5.05 [1.59–16.0] 0.006
Cardiovascular disease at admission 1.23 [0.58–2.63] 0.592
Hydration status 0.55 [0.27–1.10] 0.077
Age 1.00 [0.98–1.02] 0.627
Sepsis 1.12 [0.56–2.23] 0.752
∗
Calculated using the chronic kidney disease epidemiology collaboration (CKD-EPI) equation and classified based on NKF-KDOQI guidelines.

thromboembolism (OR 5.05; 95% CI 1.59 to 16.0, 𝑝 = 0.006). routine clinical measures, our patients apparently did not
(Table 3). have AKI on admission. The present study showed that 16% of
Regarding outcomes, the overall mortality rate was 7.5% nonsurgical patients developed AKI within five days of hos-
(𝑛 = 30); the mortality rate among patients with EAKI was pitalization. Such a finding is difficult to interpret when com-
21.9% (𝑛 = 14), and the following mortality rates were pared with the international literature. First, the operational
assessed according to the KDIGO criteria of AKI severity: definitions of AKI vary by year of publication (especially
18.5% (𝑛 = 10) for KDIGO 1, 25% (𝑛 = 2) for KDIGO 2, before or after the RIFLE consensus, AKIN, and KDIGO)
and 100% (𝑛 = 2) for KDIGO 3. Increased associations with [5, 17, 18]. Second, each clinical stage and study population is
in-hospital death (OR 5.6; 95% CI 2.36 to 13.0, 𝑝 < 0.001) different (e.g., medical and/or surgical and CA-AKI and ICU
and dialysis requirement (OR 16.5; 95% CI 1.28 to 867.2, patients), and AKI was only assessed during early hospi-
𝑝 = 0.0012) occurred among patients who developed EAKI. talization without identifying the incidence throughout the
The median length of hospital stay of patients with EAKI was hospital stay.
8 (IQR 5–14), in contrast to 6 (IQR 4–10), among patients The worldwide pooled incidence rates of hospital-
who did not develop the condition (𝑝 = 0.008) (for details acquired AKI range from 17.2% to 25.2%, with high hetero-
on hospital stay by EAKI and death, see Table 2 of the geneity among the studies analyzed in the meta-analysis by
Supplementary Material). Susantitaphong et al. [15]. This incidence is similar to that
reported in the present cohort study, despite including no
4. Discussion surgical patients and only cases of AKI diagnosed within five
days of hospitalization. Therefore, patients managed by the
The present cohort study aimed to estimate the incidence of Internal Medicine specialty without apparent AKI on admis-
AKI in nonsurgical patients detected during early hospital- sion may be a population vulnerable to the development of
ization and to identify the associated risk factors. Under AKI during early hospitalization, possibly because AKI
6 International Journal of Nephrology

patients are older and have high associated morbidity, which On the other hand, with regard to the relation between
underlines the importance of performing early screening and VTE and AKI, it should be interpreted carefully because the
monitoring in the first days of hospitalization. number of patients with VTE is small in the cohort for the
Conversely, 84% of EAKI cases in the present study corre- present study; however, kidney failure in VTE has already
spond to a KDIGO 1 (“mild” AKI) classification, with an been described in other publications and it might occur due
18.5% mortality rate, which highlights the existing link be- to the concomitant heart failure (cardiorenal syndrome), hy-
tween slight increases in serum creatinine levels and mor- poperfusion, and administration of contrast media for the
tality rate, as shown by other authors [19–21]. This issue is diagnosis through angiotomography [32].
controversial, given the recent evidence suggesting the exis- A recent study on the global overview of AKI (0 by 25
tence of a high rate of false-positive AKI cases only diagnosed initiative) [33] showed that hypotension and shock were
the most common causes of AKI in countries such as ours
based on an absolute increase in creatinine levels ≥0.3 mg/dL,
(medium-high per capita income stratum in 2014). Both enti-
particularly in a population with CKD [22]. Furthermore,
ties have clinical conditions with multiple causes, including
these values may be affected by hydration status and/or fluid sepsis. In our hospital, hypotensive patients and/or septic
replacement without implying AKI [23]. This dilemma will shock patients are managed in the ICU; therefore, they were
most likely be resolved when we have the capacity to routinely excluded from our study. Based on the third international
use molecular markers of EAKI [4, 24]. consensus defining sepsis and septic shock published after
The seminal studies by Hou et al. [25] and Shusterman et our study design and data collection [34], the “infected
al. [26] showed that the volume depletion, treatment with patients” in our cohort who developed AKI have organ dys-
aminoglycosides, contrast media, heart failure, and septic function and are, therefore, true septic patients according to
shock increased the risk for AKI in a medical-surgical popu- the new consensus.
lation. However, it should be considered that those studies The present study contributes to bridging the gap in
were conducted at least three decades ago, using different AKI scientific research on the subject of AKI in Latin American
definition criteria from those currently used, only detecting and/or developing countries [15, 35, 36]. Addressing the
epidemiology of AKI in nonsurgical patients is a great chal-
patients with severe renal injury and overlooking those with a
lenge, given the wide heterogeneity in study definition and
lesser degree of renal injury. In contrast, treatment with ami-
design, whose results become difficult to compare; most
noglycosides is uncommon in the Internal Medicine Depart-
original articles on AKI focus on cardiovascular surgery and
ment, thus lacking a key role in the present cohort study.
critical care units [20, 36–39], whereas the others focus on
Conversely, the failure to identify a relationship between specific clinical conditions, including pneumonia, renal
EAKI and the administration of nephrotoxic drugs could be transplantation, tropical diseases, and even the CA-AKI [40,
explained because the condition was only assessed within 41].
five days of hospitalization and requires later screening to be Optimal patient inclusion and in-hospital prospective
detected by variations in serum creatinine levels. However, we monitoring for EAKI incidence estimation and correct differ-
do not rule out the hypothesis that the attending physicians entiation between patients with CKD without exacerbation
were sensitized at the beginning of our study, which may have on admission and patients with CA-AKI are among the
changed their nephrotoxic drug prescribing habits. strengths of this study. Although CA-AKI was not a study
However, the main risk factor for developing EAKI on endpoint, remarkably, it is the leading cause of patient exclu-
admission is CKD from stage 3 onwards. This association sion from our cohort and accounts for 19.8% (𝑛 = 239) of
between AKI and CKD is quite complex and has been well all patients evaluated. This issue will be the focus of further
described. CKD increases the risk for AKI [14, 27–29]; AKI research.
causes CKD, and both entities share risk factors for its devel- Our study has several limitations. This study was single-
opment [30, 31]. The results from our cohort study corrobo- center in design, which limits its external validity because
rate such a relationship between the two entities and highlight disease behavior may vary depending on and according to
the importance of screening and preventive measures in healthcare center, region, or country [33]. Furthermore, no
patients with decreased GFR on admission. outcome monitoring was performed beyond the period of
Another important aspect to discuss is the scarce litera- hospitalization. Therefore, key data, including the incidence
ture that has assessed AKI risk in patients with CKD stages of CKD after EAKI, mortality rate, and end-stage renal dis-
ease (ESRD), are unknown. Conversely, hydration status on
1 and 2 (GFR ≥ 60 mL/min/1.73 m2 with structural or func-
admission was only assessed based on the attending physi-
tional kidney abnormality), being uncertain of the role of
cian’s clinical criteria, and no objective evaluation was per-
these early stages as a risk factor for AKI. Even in risk studies formed using tools such as bioelectrical impedance analysis.
of AKI in CKD, such as that by Hsu et al., GFR ≥ 60 mL/ Based on this study, we are currently working towards
min/1.73 m2 is the point of reference of “normality” to be providing the patient wellness program with good practice
compared with those having GFR < 60 mL/min/1.73 m2 . No guides for the prevention and detection of AKI, seeking to
relation was found between stages 1 and 2 of CKD (GFR ≥ strengthen the “hospital free of preventable AKI” project. The
60 mL/min/1.73 m2 with structural or functional kidney ab- AKI detection strategy used in our study can serve to guide
normality) and AKI in the results for the cohort of the present other hospital centers in the promotion of pertinent medical
study. interventions, such as how to maintain adequate hydration,
International Journal of Nephrology 7

improve the prescription writing habits of physicians (avoid- [8] S. M. Bagshaw, C. George, and R. Bellomo, “Early acute kidney
ing the indiscriminate use of nephrotoxic drugs), and solicit injury and sepsis: a multicentre evaluation,” Critical Care, vol.
the evaluation of a nephrology specialist in a timely manner. 12, no. 2, article R47, 2008.
In conclusion, the incidence of AKI detected within [9] M. Plataki, K. Kashani, J. Cabello-Garza et al., “Predictors of
five days of hospitalization in the nonsurgical population acute kidney injury in septic shock patients: an observational
and without apparent AKI on admission is similar to that cohort study,” Clinical Journal of the American Society of
reported in the international literature and is associated with Nephrology, vol. 6, no. 7, pp. 1744–1751, 2011.
prolonged hospital stay, in-hospital death, and dialysis [10] S. Finlay, B. Bray, A. J. Lewington et al., “Identification of risk
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and A. S. Go, “The risk of acute renal failure in patients with
The authors declare no conflicts of interest regarding the chronic kidney disease,” Kidney International, vol. 74, no. 1, pp.
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of Nephrology, vol. 8, no. 9, pp. 1482–1493, 2013.
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