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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2012  |  Volume : 23  |  Issue : 1  |  Page : 68-77
Hospital-acquired acute kidney injury in critically ill children and adolescents

1 Pediatric Nephrology and Hypertension Unit, Obafemi Awolowo University Teaching Hospitals Complex, Ile-Ife, Osun State, Nigeria
2 Department of Demography and Social Statistics, Obafemi Awolowo University Ile-Ife, Osun State, Nigeria

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Date of Web Publication3-Jan-2012


This study determined the (1) hospital incidence, prevalence and etiology; (2) frequency of each of the acute kidney injury (AKI) stages and (3) the 60-day outcome. Retrospective analysis of clinico-laboratory data of Nigerian children/adolescents with hospital-acquired acute kidney injury (hAKI) was performed. AKI occurred in 103 (3.13%) of 3,286 childhood and adolescent admissions. Twenty-eight (27.2%) were hAKI while 72.8% were community-acquired AKI (cAKI). Annual hAKI incidence and prevalence rates were 0.17% (or 3.7 per million children population [pmcp] / year) and 0.84% (or 18.3 pmcp), respectively. Male (20):female (8) ratio was 2.5:1. In the hAKI group, median age was 5 (0.063-15.0) years. AKI stages 1, 2 and 3 accounted for 14.3%, 25.0% and 60.7%, respectively. AKI stage 3 was most anuric, with high dialysis requirement (P = 0.0329). Nephrotoxics (42.87%) were a leading cause of hAKI. Seventy-five percent of the recorded deaths were in the first 28 hAKI days. Median survival time was 23.5 admission (11-52) days. The means values of maximum serum creatinine (Scr) for survivors (486.0 ± 382.0 μmol/L or 5.5 ± 4.3 mg/dL) and for non-survivors (353.0 ± 160.0 μmol/L or 4.0 ± 1.8 mg/dL) were similar (P > 0.20). The 60-day cumulative mortality was 36.7%. Scr severity may not be a reliable mortality determinant among AKI patients. The maximal mortality in the first 28 days of hAKI onset and overall high mortality rate indicate that high level of clinical vigilance and informed therapeutic intervention will be critical to survival during this period. Cause of death was multi-factorial.

How to cite this article:
Olowu WA, Adefehinti O, Bisiriyu AL. Hospital-acquired acute kidney injury in critically ill children and adolescents. Saudi J Kidney Dis Transpl 2012;23:68-77

How to cite this URL:
Olowu WA, Adefehinti O, Bisiriyu AL. Hospital-acquired acute kidney injury in critically ill children and adolescents. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2022 Aug 16];23:68-77. Available from: https://www.sjkdt.org/text.asp?2012/23/1/68/91305

   Introduction Top

Acute kidney injury (AKI) is an abrupt clinical and / or laboratory manifestation of abnormal kidney function within 48 h of bilateral kidney insult of any kind. The term AKI was introduced by the International Consensus Conference on Acute Dialysis Quality Initiative (ADQI) workgroup. [1] It replaces the highly restrictive but popular term, acute renal failure (ARF). AKI is a clinical syndrome with different severity levels of acute kidney dysfunction. The Acute Kidney Injury Network (AKIN) workgroup [2] , a sub-committee of ADQI, recently classified AKI into three increasing severity stages (AKI stages 1 to 3) of kidney dysfunction based on the ADQI work-group's RIFLE criteria with modifications. [1] The acronym RIFLE refers to risk (AKI stage 1), injury (AKI stage 2), failure (AKI stage 3), loss of kidney function and end-stage renal disease (ESRD). This serious disorder has the potential for progression to irreversible loss of kidney function or ESRD. [1] Progression may be rapid and severe in those with pre-existing kidney disease. Before now, emphasis had been laid on the severest level of acute kidney dysfunction, simply referred to as ARF. The early and less-clinically obvious phases of acute kidney damage (AKI stages 1 and 2), which can significantly multiply morbidity and mortality in the critically ill if not recognized and treated early, are often missed. Undetected early AKI stages can easily evolve into stage 3 AKI (renal failure) ─ a stage commonly associated with high morbidity and mortality rates [3],[4],[5],[6],[7],[8] and, significantly, very high demand on dialysis facility, [3],[9] which many patients in this country cannot afford. [4],[9]

AKI is both community and hospital acquired. Although birth asphyxia-related hospital-acquired AKI (hAKI) has been reported in this country, [11],[12] data on childhood and adolescent hAKI are generally scarce from Africa as previous reports on AKI had focused mainly on community-acquired AKI (cAKI). [3],[4],[13],[14],[15] cAKI is more common in developing countries with infections, diarrhea and vomiting and acute glomerulonephritis being more frequently causative and, in addition, in our area, Burkitt's cell lymphoma nephropathy [3],[4],[13],[14],[15],[16],[17] when compared with developed nations where hAKI is more prevalent. [6],[7],[8],[18] Cardiopulmonary bypass surgery, bone marrow transplantation, nephrotoxic medications, nosocomial infection and multiple organ failures in the critically ill patients commonly cause hAKI in developed countries. [7],[8],[18],[19],[20],[21],[22],[23],[24] Using the new AKI diagnostic definition and staging system by AKIN, [2] we determined the hospital incidence and prevalence, frequency of each of the AKI stages, etiology and clinical outcome of childhood and adolescent hAKI in southwestern Nigeria.

   Patients and Methods Top

Clinical charts of patients managed for AKI in the pediatric surgical ward, intensive care unit and pediatric nephrology and hypertension unit of our hospital were retrospectively reviewed for the first 60 days of follow-up starting from the hAKI-onset date. The study period ranged between June 2004 and June 2008. Our hospital caters for the healthcare needs of 1,530,000 children (<13 years) and adolescents (13-17 years) in Osun State, southwestern Nigeria. Our hospital's Ethics and Research Committee approved the research protocol.

Analyzed data were age, gender, anthropometry, vital signs, admission diagnosis, admission date and duration, hAKI duration before diagnosis, hAKI stage at onset and at peak of injury, urine output and management outcome of a 60-day follow-up. Relevant laboratory investigations including serum creatinine (Scr), both at baseline and at follow-up, were reviewed.


AKI was diagnosed based on the AKIN criteria [2] as an absolute increase in Scr level within 48 h of bilateral kidney insult by ≥0.3 mg/dL (≥26.4 μmol/L) or a 50% (1.5-fold) increase in Scr or more from the baseline. We determined the duration of kidney injury from the interval between the last time urine was observed to be of normal volume and the time it was observed to be diminished or the time interval between surgical intervention or administration of nephrotoxic agent and AKI onset. AKI was staged using the creatinine criteria of the AKIN work-group [2] -Stage 1 AKI (AKI-1): rise in Scr by ≥0.3 mg/dL (26.4 μmol/L) or an increase of >150-200% (1.5-2-fold increase) from baseline; Stage 2 AKI (AKI-2): rise in Scr by >200-300% (>2-3-fold increase) from baseline; Stage 3 AKI (AKI-3): rise in Scr by >300% (>3-fold) from baseline or Scr ≥4.0 mg/dL (≥354 μmol/L) with an acute rise of at least 0.5 mg/dL (44 μmol/L). Because both the RIFLE and the AKIN criteria failed to define non oliguric AKI (NOAKI), NOAKI was defined as urine output that was persistently >0.5 mL/kg/h in the setting of an abnormal Scr level. Similarly, anuric AKI (ANAKI) was defined as urine output that was <0.039 mL/kg/h for 12 h or more. Although AKI was staged at the time of diagnosis, the maximum Scr (maxScr) level reached in each patient was used for the final AKI staging. maxScr was defined as the highest Scr level reached in any patient either before death or before gradual return to normal in survivors. Time to maxScr was determined from the time interval between the first Scr determination following diagnosis and the time the maxScr was determined. Those who were initially diagnosed AKI-1 or AKI-2 but later required dialyses were upgraded to AKI-3 as recommended. [2] hAKI was defined as onset of AKI in a hospitalized patient who, at the time of admission, showed no evidence of AKI (reduced urine output or elevated Scr).

ADQI [1] recommended that normal estimated glomerular filtration rate (eGFR) ranging from 75 to 100 mL/min per 1.73 m 2 should be used in those who do not have baseline Scr measurement; a theoretical baseline Scr value can then be obtained from the simplified Modification of Diet in Renal Disease (MDRD) study's predictive eGFR equation with corrections for age, gender and race. [25] In this study, all patients without baseline measure of renal function but had spent at least one week on admission before hAKI onset were assumed to have eGFR value of 100 mL/min/1.73 m 2 . By the MDRD equation, eGFR = 186 × ([Scr] -1.154 × age-0.203 × 0.742 (if female) × 1.210 (if black). [25] The inclusion criteria were hospitalized children and adolescents without clinical evidence of AKI at baseline, with normal baseline Scr or eGFR but who later developed AKI following either therapeutic intervention, surgery, nosocomial infection or any other severe clinical conditions. Patients with known chronic kidney disease, abnormal baseline Scr or eGFR and/or diminished urine output at baseline were excluded. Where doubts existed about whether or not a case of AKI was hospital acquired, such a case was classified as community acquired.

Systemic co-morbidities were analyzed for impact on outcome. maxScr and maximum serum urea (maxSur) were correlated with clinical outcome. Survival time was defined as the period ranging between hAKI onset and death.

   Statistical Analysis Top

Data analyses were performed using both descriptive and comparative statistics. Descriptive statistics used comprised mean, standard deviation (SD), median, percentages and proportions. The comparative statistics were chi-square test, Fisher's exact test, student's t-test, odds ratio, regression analysis, correlation coefficient, Kaplan-Meier survival analysis, and the log-rank test using the SPSS 15.0 for Window evaluation version (2006 SPSS Inc.). A 60-day survival analysis for the three AKI stages using the Kaplan-Meier statistics and the log rank test were performed.

   Results Top

AKI was diagnosed in 103 of 3,286 (3.13%) admitted children and adolescents. Twenty-eight (27.2%) were hAKI while cAKI accounted for the remaining 72.8% (P = 0.0002). The overall annual hospital incidence of AKI was 0.63% (or 13.5 per million children population [pmcp]/year); annual hAKI and cAKI incidence rates were 0.17% (or 3.7 pmcp/year) and 0.46% (or 9.8 pmcp/year), respectively. The overall hospital prevalence of AKI was 3.07% (or 67.5 pmcp). hAKI and cAKI prevalence rates were 0.84% (or 18.3 pmcp) and 2.23% (or 49.2 pmcp), respectively. Twenty of 28 hAKI patients were males (male:female ratio 2.5:1; P = 0.0278). The median age for hAKI was 5 (0.063-15.0) years. Thirteen of 28 (46.4%) hAKI patients were under 5 years of age. The pre-AKI admission diagnoses are summarized in [Table 1]. Mean admission time to hAKI onset period was 252 ± 292 (14- 1008) h. hAKI was diagnosed 22.25 ± 11.65 (5-48) h after onset. Mean Scr at baseline, at AKI onset and at peak of hAKI injury (maxScr) were 59.0 ± 15.0 (0.67 ± 0.17 mg/dL), 272.0 ± 176.0 (3.1 ± 2.0 mg/dL) and 448.0 ± 340.0 (5.1 ± 3.8 mg/dL) μmol/L, respectively. The difference between the means of Scr at peak of AKI and AKI onset was significant (P < 0.01). Overall median time to maxScr from hAKI diagnosis was 60 (range 24-768) h. [Figure 1] shows the cumulative frequency distribution of times to maxScr in each of the three hAKI stages. Acute progression of kidney injury from either stage 1 or 2 to the next severe hAKI stage occurred in 13 of 19 (68.42%) patients [Figure 2]. Although the odds of progression from one stage to the next severe stage was 1.7-times higher in hAKI-1 than in hAKI-2, it failed to reach statistical significance (95% CI: 0.19-15.4; P = 0.3689). hAKI-3 was significantly the most common stage of hAKI at the peak of injury ([Figure 2]; P = 0.007) and the most frequently associated with anuria [Table 2]. All the six (21.4%) patients who required dialysis had hAKI-3 and were oligoanuric. Compared with hAKI-1 and hAKI-2, hAKI-3 patients were significantly more likely to require dialysis treatment (P = 0.0329). The median duration of oligoanuria in OAKI and ANAKI was 6 (1-14) days; 14 of 19 (74%) significantly reached the diuretic phase within 10 days (P = 0.0394) and all patients were in diuresis by the end of hAKI day 14.
Figure 1: Cumulative frequency plots of time to maximum serum creatinine (maxScr) for each of the
hospital-acquired acute kidney injury (hAKI) stages show that time to maxScr was shortest with hAKI– 1. Median time to maxScr was 24 h, 48 h and 96 h for hAKI– 1, hAKI– 2 and hAKI– 3, respectively.

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Figure 2: Flow chart showing the onset prevalence of each of the hospital-acquired acute kidney injury stages (hAKI) and progression from one stage to the next severe stage.

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Table 1: Admission diagnosis before acute kidney injury (AKI) onset.

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Table 2: Relations between acute kidney injury (AKI) type and AKI stage.

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Nephrotoxicity (42.87%) was significantly the leading cause of hAKI (P = 0.002; [Figure 3]). The suspected risk factors for hAKI are shown in [Table 3]. Co-morbid conditions were highly prevalent, with 25 of 28 hAKI patients being significantly associated with two or more co-morbidities (P = 0.0000). Hemato-oncologic co-morbidities were the most prevalent [Table 4]. Overall, the co-morbidities impacted similarly on survival, P = 0.382. Similarly, cross-tabulation comparisons between two different comorbidities on mortality from AKI using proteinuria as the reference yielded no significant difference, [Table 4]. [Figure 4] summarizes the final proportion of patients and survival pattern in each of the hAKI stages at the peak of injury. [Figure 5] shows the 60-day survival curve of all hAKI patients (63.3%); survival times and proportions surviving were similar in hAKI 1, 2 and 3 (log rank P = 0.451, [Figure 6]). Six patients died within the first 28 days of hAKI onset while two patients died later (P = 0.005); the respective 28-day and 60-day cumulative mortality rates were 25.2% and 36.7%. Four deaths (50.0%) were associated with septicemia-related hAKI; one death (12.5%) each was associated with thrombotic thrombocytopenic purpura, diuretic, cytotoxics and surgery-related hAKI. Mortality was similar in children <5 years and >5 years of age (P = 0.1884). The difference between the maxScr means for survivors (486.0 ± 382.0 μmol/L or 5.5 ± 4.3 mg/dL) and non-survivors (353.0 ± 160.0 μmol/L or 4.0 ± 1.8 mg/dL) failed to differ significantly (P > 0.20). Similarly, the positive correlation observed between mortality and maxScr (r = +0.656) was not statistically significant (P = 0.078). However, there was a significant positive correlation between mortality and maxSur attained (r = +0.949; P = 0.0000) in the patients. The mean Scr, 60.6 ± 13.2 (48-88) μmol/L or 0.69 ± 0.15 (0.54- 0.99) mg/dL, was within the normal range by day 32 of onset of the hAKI in all 18 patients that survived the illness.
Figure 3: Prevalence of each of the etiologies of hospital-acquired acute kidney injury (hAKI). Surgical procedures associated with hAKI were nephrectomy for nephroblastoma (n = 2), exploratory laparotomy for intussusceptions (n = 1) and burr hole in severe head injury (n = 1).

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Figure 4: Flow chart showing the prevalence of each of the hAKI stages at the peak of injury and outcome in each of the stages.

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Figure 5: Kaplan– Meier survival curve of all hospital-acquired acute kidney injury (hAKI) patients (n = 28). The cumulative survival probability at 14, 28 and 60 days was 96.4%, 74.8% and 63.3%, respectively. Numbers of patients at risk at the beginning of each survival time interval are shown.

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Figure 6: Kaplan– Meier survival curves of each of the hospital-acquired acute kidney injury (hAKI) stages. The cumulative survival probability for hAKI– 1, hAKI– 2 and hAKI– 3 at 14 days were 100%, 100% and 94.1%, respectively, while the corresponding survival probabilities at 28 days were 100%, 71.4% and 70.6%, respectively. The survival probabilities at the end of 60 days were 100%, 53.6% and 60.5%, respectively. The numbers of patients at risk at the beginning of each survival time interval are shown for each of the hAKI stages.

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Table 3: Suspected risk factors for hospital-acquired acute kidney injury (hAKI) and interventions that
precipitated hAKI in some of the patients (n = 23).

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Table 4: Comorbidities and outcome in all patients.

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   Discussion Top

Pediatric hAKI studies from developed countries revealed incidence rates that ranged between 2.5 and 30%. [6],[8],[26],[27],[28],[29] These are much higher than the 0.17% (or 3.7 pmcp/year) hAKI incidence found in this study. The low incidence possibly reflects the retrospective nature of this study. Some cases would have been probably missed, because they were not diagnosed as AKI. It could also be due to the fact that complex procedures, namely cardiopulmonary bypass surgery, bone marrow and solid organ transplantation requiring increased exposure to nephrotoxic medications in critically ill children, are not currently performed in our center. These procedures are common in developed countries, and are frequently associated with hAKI. [6],[8],[19],[20],[21],[22],[23] This study shows that the overall AKI incidence has increased in our unit from 10 pmcp/year (1995-1999) [9] to 13.5 pmcp/year (2004-2008) thus reflecting the general global rising trend of AKI. [6],[7],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29] Compared with cAKI in this study, hAKI incidence was significantly 2.7-times less common. This agrees with the fact that cAKI is seen more commonly than hAKI in developing countries when compared with developed countries, where hAKI is seen more commonly. [6],[7],[8],[18] The huge overall AKI prevalence rate of 67.5 pmcp in this study should be a cause for concern in this part of the country as this is bound to translate to high cost of AKI funding on one side and overall healthcare cost in general.

The kidney injured patient may not manifest clinical symptoms or elevated Scr for days after the injury. By the time Scr is elevated, the patient is usually very sick, with several co-morbidities competing to terminate life, and mortality is usually very high. [3] Going by the AKIN workgroup staging criteria for AKI, [2] this study demonstrated advanced kidney injury at the time of diagnosis. This was reflected in the percentage increase of 361.0% in the mean Scr from the baseline (from 59 to 272 μmol/L). This further demonstrates the inadequacy of Scr as a marker of AKI, as injury would have been far advanced before detection; that a slight rise in Scr level that was as low as 0.3 mg/dL (26.5 μmol/L) was associated with significant kidney damage, high morbidity and mortality from AKI [31] points to the need for early diagnosis that is presently not possible with Scr. Early AKI diagnosis and treatment may limit morbidity multiplication, disease progression and dialysis requirement and reduce mortality from this potentially fatal disorder. Biological markers that are capable of revealing AKI within few hours of kidney insult, namely plasma neutrophil gelatinase-associated lipocalin (NGAL), plasma cystatin C, urine NGAL, urine interleukin-18 (IL-18), urine kidney injury molecule-1 (KIM-1) [32] and urine liver fatty acid-binding protein (L-FABP, rising within 4 h of injury) [33] although still in the experimental and research stages, appear promising in this regard. Majority of the patients were in the hAKI-1 stage (50%) at the time of diagnosis, but at the peak of injury, hAKI-3 (61%) was significantly the predominant stage. This reflects the dynamic nature of AKI; its progression from one AKI stage to the next severe AKI stage occurred within few hours of injury onset (median time to maxScr: 60 h). The time to maxScr was shortest with AKI-1 (median, 24 h), while it was the longest with AKI-3 (median, 96 h)-[Figure 1]. The risk of progression was, however, similar in both hAKI-1 and hAKI-2 (95% CI: 0.19- 15.4). hAKI-3 was significantly the most anuric and dialysis requiring of all the three AKI stages, indicating the need for a therapeutic protocol that may abort progression to this level of injury. This is of special importance to resource-poor countries, where dialysis access is still grossly inadequate. [3],[4],[9],[13],[14],[15],[16],[[17] Nephrotoxics were the significant major causative agents in this study; these nephrotoxics were diuretics, angiotensin-converting enzyme inhibitors (ACEI) and cytotoxic drugs used for the prevention of fluid overload during blood transfusions, treatment of nephrotic proteinuria and cyto-reductive therapy in Burkitt's lymphoma patients. Nephrotoxics are well-known documented etiologies of hAKI, but are rarely the most frequent cause of hAKI in the literature. [6],[34] Some of the factors that were suspected to have provoked AKI in our patients following treatment with diuretics, ACEI and cytotoxic drugs were as listed in [Table 3]. Careful assessment of patients for any of these factors and correction before instituting these therapies will significantly reduce the incidence of nephrotoxics-associated hAKI.

AKI remains a source of concern, given its high morbidity and mortality rates. [3],[4],[7],[13],[14],[15],[16],[17],[29] Comorbidities occur commonly in AKI, and are important risk factors for mortality. [3],[16],[35] In this study, all patients had one form of comorbidity or the other; onco-hematologic condi­tions were the most prevalent. All comorbidities impacted similarly on outcome, suggesting that all co-morbidities should be treated with an equal degree of aggression. Failure of the co-morbidities to impact significantly on outcome might be due to hospital onset of the AKI and diagnosis within 48 h and early treatment that modified the naturally aggressive behavior of the co-morbidities. Seventy-five percent of the recorded deaths were within the first 28 days of hAKI onset. Aggressive management and high level of clinical vigilance in the first 28 days of hAKI onset may therefore be critical to survival, as mortality was significantly maximal during the period. We failed to identify a significant risk factor for mortality in the patients except for rising serum urea that correlated significantly with mortality; mortality was probably multi-factorial. Mean Scr among survivors and non-survivors was not significantly different. A recent study from South Africa failed to demonstrate any significant difference in mean Scr among survivors and non-survivors, but found serum urea to be a significant risk factor for mortality. [16] By implication, Scr may not be a reliable mortality determinant in AKI patients. All hAKI stages demonstrated similar survival times, meaning that all hAKI patients should be treated with equal zeal.

hAKI was approximately three-times less common than cAKI. Compared with other etiologies, nephrotoxics significantly caused hAKI most frequently. The case fatality rate from nephrotoxics was low compared with septicemia-related AKI. Scr severity was not significantly correlated with mortality and may, therefore, not be a reliable mortality determinant among AKI patients. In view of the high mortality in this study and maximal mortality in the first 28 days of hAKI onset, a high level of clinical vigilance and informed therapeutic intervention will be critical to survival during this period in any patient with AKI; cause of death was probably multi-factorial.

   Acknowledgment Top

This paper was presented in an abstract form at the 10th Congress of the African Association of Nephrology held in Abuja, Nigeria (February 16-19, 2009). There are no financial interests to declare.

   References Top

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35.Werner HA, Wensley DF, Lirenman DS, Leblanc JG. Peritoneal dialysis in children after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1997;113:64-70.  Back to cited text no. 35

Correspondence Address:
Wasiu Adekunle Olowu
Pediatric Nephrology and Hypertension Unit, Obafemi Awolowo University Teaching Hospitals Complex, PMB 5538, Ile-Ife, Osun State
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Source of Support: None, Conflict of Interest: None

PMID: 22237222

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]

  [Table 1], [Table 2], [Table 3], [Table 4]


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