|Year : 2017 | Volume
| Issue : 4 | Page : 240-244
Incidence and predictors of acute kidney injury in birth asphyxia in a Tertiary Care Hospital
Muhammed Aslam, Sugandha Arya, Harish Chellani, Charanjeet Kaur
Department of Pediatrics and Biochemistry, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India
|Date of Web Publication||17-Oct-2017|
Department of Pediatrics, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi - 110 029
Source of Support: None, Conflict of Interest: None
Objective: The objective of this study is to estimate the incidence of acute kidney injury (AKI) in birth asphyxia and to find out the predictors of AKI in birth asphyxia in a tertiary care hospital. Materials and Methods: This is a cross-sectional study conducted in the neonatal intensive care unit of a tertiary care center in Northern India during November 2014– October 2015. Inborn babies admitted here with severe birth asphyxia were included in the study. The neonates were evaluated for the evidence of AKI and were grouped into two groups: Group I (all neonates with severe birth asphyxia as per the WHO definition and having evidence of AKI) and Group II (all neonates with severe birth asphyxia as per the WHO definition and without having evidence of AKI). Those with congenital renal anomalies were excluded from the study. The two groups were then compared. AKI network definition was used to define AKI. Results: The incidence of AKI in the present study was 44.21%. There was no significant difference in incidence between term and preterm neonates, and among various stages of hypoxic-ischemic encephalopathy. The majority (95%) had nonoliguric renal failure. Most (92.8%) of the cases recovered before discharge and the rest recovered at 1 month follow-up. Prolonged labor was found to be significantly associated with AKI. Patients with shock had more advanced stages of AKI compared to those without shock. Conclusion: From this study, it can be inferred that it is difficult to predict AKI based on clinical features such as oliguria or Apgar score, and it is better to screen all the birth asphyxia cases for AKI so that they can be detected early and managed accordingly. In addition, a single normal value of blood urea/serum creatinine cannot exclude AKI, and serial monitoring is important. Shock should be detected early and treated aggressively as shock was associated with advanced stages of AKI.
Keywords: Acute kidney injury, acute renal failure, birth asphyxia, perinatal asphyxia
|How to cite this article:|
Aslam M, Arya S, Chellani H, Kaur C. Incidence and predictors of acute kidney injury in birth asphyxia in a Tertiary Care Hospital. J Clin Neonatol 2017;6:240-4
|How to cite this URL:|
Aslam M, Arya S, Chellani H, Kaur C. Incidence and predictors of acute kidney injury in birth asphyxia in a Tertiary Care Hospital. J Clin Neonatol [serial online] 2017 [cited 2021 Oct 28];6:240-4. Available from: https://www.jcnonweb.com/text.asp?2017/6/4/240/216910
| Introduction|| |
Birth asphyxia is a common problem in neonatal intensive care units and is a significant cause of morbidity and mortality. Overall, the incidence of birth asphyxia is reported to vary from 1 to 10 per 1000 live births., Asphyxia can lead to redistribution of cardiac output to vital organs while potentially compromising renal, gastrointestinal, and skin perfusion, and occasionally to multiorgan dysfunction. Acute kidney injury (AKI) is more common in asphyxiated neonates, and this can adversely affect the overall prognosis.
As kidneys are very sensitive to hypoxia, renal insufficiency can occur within 24 h of a hypoxic insult, which if prolonged, may lead to irreversible injury. AKI is characterized by a sudden impairment of renal function that results in altered fluid, electrolyte, and acid-base balance. It affects 8%–24% of critically ill neonates and has a mortality rate of 10%–61%. The common conditions contributing to kidney injury in the neonatal period include neonatal sepsis, birth asphyxia, respiratory distress syndrome, dehydration, heart failure, and urologic anomalies, the first two being the most common causes.,,,,,
Even though birth asphyxia is one of the most common causes of renal failure in neonatal population, the actual incidence is not well-known. This is because, we usually suspect renal failure when a patient develops oliguria, and up to 33% cases of AKI in neonates are nonoliguric. Identified risk factors suggest that AKI occurs more commonly in association with systemic diseases than primary renal disease. It has been observed that one-third of critically ill children develop AKI, which is four-fold higher than noncritically ill children. AKI has been associated with prolonged hospital stay. AKI is an independent risk factor for poor outcome in critically ill neonates. In addition, children who survive ARF are likely to experience residual renal abnormalities. The first step of prevention and treatment of neonatal AKI is to identify infants at high risk and detecting AKI early so that further damage can be prevented.
The initial definitions of renal failure were based on blood urea nitrogen which is affected by other factors such as dehydration, steroid usage, and metabolic status. Multiple definitions had been used previously, leading to confusion in literature and difficulty in comparison among studies. Later, a multilevel classification system known as the Risk, injury, failure, loss, end-stage kidney disease (RIFLE) criteria was developed for ARF. It was based on estimated creatinine clearance, serum creatinine, and oliguria. The latest definition is based on AKI network (AKIN) criteria.
A number of small single-centered studies have reported AKI in 30% to 56% of term babies with birth asphyxia.,,, This number is probably an under estimate given the limitations of the diagnostic criteria used. These studies defined AKI based on serum creatinine level and urine output. However, up to 1/3rd of the cases of AKI in neonates are nonoliguric. The present study has been planned to determine the incidence and risk factors of AKI in neonates with birth asphyxia.
| Materials and Methods|| |
This is a cross-sectional study conducted at Neonatal division of the Department of Paediatrics in collaboration with Department of Biochemistry of Vardhaman Mahavir Medical College and Safdarjung Hospital, New Delhi. Approval of Ethical Committee of the institution was taken. The details of the study method were properly explained, and a printed information sheet in the local language was provided to the parents. They were included in the study after obtaining an informed written consent. The sample size was calculated using the formula n = 4P (100-P)/d 2 where 'n' is sample size, “P” is anticipated incidence of AKI in birth asphyxia and 'd' is absolute precision which was taken as 10%. The sample size was found to be 85 on the basis of incidence of AKI in asphyxiated neonates from previous studies. Inborn babies admitted to the neonatal unit having severe birth asphyxia as per the WHO definition  were included in the study. Neonates with congenital renal anomalies as detected by antenatal or postnatal ultrasonogram and neonates with other confounding factor believed to alter renal function such as septicemia, respiratory distress syndrome, necrotizing enterocolitis, and major congenital anomalies were excluded from the study. Baseline maternal data (including age, any medical illnesses, Hb, number antenatal visits, obstetric history, and gestation) were collected. Baseline neonatal details including gestational age, APGAR score, birth weight, and resuscitation details were also recorded. Serum creatinine and blood urea were measured for all these neonates on the first 3 consecutive days of illness. Urine output was recorded, using diaper weight method. All neonates were assessed and staged for hypoxic-ischemic encephalopathy (HIE) using Sarnat and Sarnat Clinical staging of HIE. The presence and severity of AKI were determined on the basis of definition given by the AKIN which is given in [Table 1]. All neonates who had AKI underwent sonography to rule out gross congenital renal anomalies. All neonates with AKI were included in Group-I and those without AKI in Group-II. The two groups were then compared.
Acute kidney injury network definition and staging of acute kidney injury
The definition of AKI followed is as shown in [Table 1].
Estimation of serum creatinine
Serum creatinine was estimated on fully automated clinical biochemistry analyzer (HITACHI 912) which uses JAFFE's method, using commercially available kits for the same.
Data analysis was done using Stata 11.2 software. Mean ± standard deviation/median (minimum-maximum) was calculated for continuous variables and frequency for categorical variables. The prevalence and 95% confidence intervals were reported. Categorical variables were compared using Chi-Square/Fisher's exact test. Continuous variables following the normal distribution between the two groups were compared by independent t-test (2 groups) or by one way ANOVA test (>2 groups). Data not following normal distribution were compared using Kruskal–Wallis/Wilcoxon rank sum test among the groups as applicable. P < 0.05 was considered statistically significant.
| Results|| |
Out of 120 cases enrolled, 25 cases were excluded later (those who met exclusion criteria or died before completion of study). The remaining 95 cases were evaluated for AKI. AKI was diagnosed in 42 newborns (44.21%) who were included in Group I (AKI group) and the remaining in Group II (non-AKI group). Variables such as maternal age, birth weight, gestational age, Apgar scores at 1 and 5 min, and duration of resuscitation were comparable between the two groups [Table 2].
|Table 2: Comparison of demographic and other variables such as Apgar scores and duration of nursery stay between the two group|
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On comparing the delivery variables, no significant differences were noted among the two groups. However, the AKI group had prolonged labor more often than the non-AKI group, and the difference was statistically significant (P< 0.05) [Table 3].
In addition, the two groups did not differ significantly in terms of gestational age, low birth weight, and appropriate for gestational age (AGA)/small for gestational age (SGA)/large for gestational age. Antibiotic usage either in the mother during the last week or in the neonate was also not found to be significantly different between the two groups.
Shock was found more frequently (26.19%) in AKI group than those without AKI (11.32%). However, the difference was not statistically significant (P = 0.06). In addition, among AKI group, neonates with shock had more sever stages of AKI compared to those without shock, the difference being statistically significant (P = 0.04) [Table 4].
The neonates in the two groups had a significant difference in initial blood urea and creatinine values at the time of admission. Contrary to the expectation, the values were lower in asphyxiated neonates with AKI, the difference being statistically significant (P< 0.05). This signifies that an initial normal blood urea/serum creatinine value cannot rule out AKI and underlines the important of serial monitoring.
With respect to morbidity duration of nursery stay, time of starting of feeds and presence and degree of HIE were compared between the two groups. Statistically significant difference was observed for none of these parameters. In addition, no relation was observed between the severity of AKI and severity of HIE. Out of the 42 cases of AKI diagnosed, 13 neonates succumbed to their illness, and one baby was taken against medical advice by parents. Although death occurred more frequently in the AKI group, the difference was not statistically significant. It is important to note that only two (4.76%) of the 42 of the neonates diagnosed to have AKI in our study had oliguria. Only three (7.14%) of the neonates had decreased renal function at the time of discharge. These neonates had decreasing trend of serum creatinine and were followed up in high-risk clinic of the hospital. Two of them had normal renal function at 1 month follow-up while one patient was lost to follow-up.
Out of the 42 cases of AKI in our study, 12 cases (28.57%) were found to be in AKI Stage 1, 9 cases (21.42%) in AKI Stage 2, and 21 cases (50%) were found to be in AKI Stage 3. Demographic data such as maternal age, gestational age, sex of the baby, and birth weight do not differ significantly among different stages of AKI.
| Discussion|| |
A number of Previous studies have been done in different parts of the world to investigate the incidence of AKI in birth asphyxia.,,, Incidence among these studies varied from 12.5% to 64%. In these studies, a uniform definition of AKI was not used, leading to lack of uniformity and comparability. In addition, risk factors for AKI were not investigated in the previous studies.
Basic demographic profile was comparable between the two groups. Univariate analysis of variables such as gender, mean birth weight, mean gestational age, mean maternal age, and resuscitation (mode and duration) at birth did not reveal any significant difference between the two groups. In our study, 44.21% of cases of severe birth asphyxia developed AKI. In a similar study conducted on ARF in asphyxiated neonates in north India by K. C. Meena et al., it was found to be 61.66%. This difference can be attributed to the fact that the diagnosis of AKI in their study was based on a single blood urea and serum creatinine level and not on the currently accepted AKIN definition (based on rising values of serum creatinine). We also found that the prevalence was not significantly different between term and preterm neonates, and Among various stages of HIE.
Prolonged labor (total duration of labor >20 h) was found more frequently in AKI group compared to non-AKI group, the difference being statistically significant (P< 0.05). This indicates that prolonged labor predisposes to AKI in birth asphyxia. This parameter had not been evaluated in any previous studies. Shock was found more frequently in asphyxiated neonates with AKI than those without AKI. However, the difference was not statistically significant (P = 0.06). In addition, among AKI group, neonates with shock had more sever stages of AKI compared to those without shock, the difference being statistically significant (P = 0.04).
An important and unexpected finding in our study is that the mean initial blood urea and serum creatinine values (done within 24 h of life) were lower in AKI group compared to non-AKI group, the difference being statistically significant (P< 0.05). This was not detected in any previous studies – either because, they evaluated only the difference between two serial values or in studies which diagnosed AKI based on single blood urea/serum creatinine values the sample was taken after 48–72 h of life. This finding has significant clinical implication-a single normal value of blood urea/serum creatinine obtained early in the neonatal period cannot exclude AKI, underlying the importance of serial monitoring (as in AKIN definition of AKI). It also signifies that the first urea and creatinine do not appear to contribute significantly to the development of AKI. This could also reflect the natural history of AKI demonstrating that AKI develops later in the illness.
AKI was not found to be significantly different among term and preterm neonates in our study. There was no significant difference in the prevalence of AKI in preterm AGA, term AGA, and SGA in our study. Maternal factors such as maternal age, ante partum hemorrhage, and meconium stained liquor did not differ significantly between the two groups. Maternal diseases such as hypertensive diseases of pregnancy and gestational diabetes also did not show significant difference.
The majority had nonoliguric renal failure. Only 2 (4.7%) of the neonates with AKI in our study had oliguric renal failure. Literature also mentions nonoliguric renal failure as being more common. In our study, 28.5% of cases were found to be in AKI Stage 1, 21.4% of cases in AKI Stage 2, and 50% of cases in AKI Stage 3. Only three of the patients (7%) were discharged with diminished renal function, and all of them had decreasing trend of serum creatinine. Two of them had normal renal function at 1 month follow-up while one patient was lost to follow-up. In our study, the mortality of neonates was found to be 31.71% within the AKI group. It was found that demographic data such as maternal age, sex of the baby, gestational age, and birth weight do not differ significantly among the different stages of AKI. It was also found that the outcome of neonates with different stages of AKI did not differ significantly among each other. In addition, stage of AKI did not show any correlation with stage of HIE.
| Conclusion|| |
From the present study, it can be inferred that it is difficult to predict AKI based on clinical features, oliguria, or Apgar score, and it is better to screen all the babies of birth asphyxia for AKI so that they can be detected early and managed accordingly. In addition, a single normal value of blood urea/serum creatinine cannot exclude AKI, and serial monitoring is important. Shock should be detected early and treated aggressively as shock is associated with advanced stages of AKI.
Needless to say, the study like any other study had limitations as follows:
- Although the sample size based on the previous studies was achieved, a complete elucidation of clinical profile of AKI could not be done because of the comparatively small sample size. Hence, a study with even a larger sample size is necessary to know the complete clinical profile of AKI in birth asphyxia
- The study reflects the clinical profile of AKI in a tertiary care hospital which may differ from the periphery. Only inborn babies were considered in this study
- Urine output was measured using diaper weight method, which may not be accurate.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
McGuire W. Perinatal asphyxia. BMJ Clin Evid 2007;2007. pii: 0320.
Askenazi D, Smith LB, Furth S, Warady BA. Acute kidney injury and chronic kidney disease. In: Avery's Diseases of the Newborn. 9th
ed. Philadelphia: Elsevier Saunders; 2012. p. 1205-21.
Andreoli SP. Acute renal failure in the newborn. Semin Perinatol 2004;28:112-23.
Mortazavi F, Hosseinpour Sakha S, Nejati N. Acute kidney failure in neonatal period. Iran J Kidney Dis 2009;3:136-40.
Mathur NB, Agarwal HS, Maria A. Acute renal failure in neonatal sepsis. Indian J Pediatr 2006;73:499-502.
Jayashree G, Saili A, Sarna MS, Dutta AK. Renal dysfunction in septicemic newborns. Indian Pediatr 1991;28:25-9.
Agras PI, Tarcan A, Baskin E, Cengiz N, Gürakan B, Saatci U. Acute renal failure in the neonatal period. Ren Fail 2004;26:305-9.
Csaicsich D, Russo-Schlaff N, Messerschmidt A, Weninger M, Pollak A, Aufricht C. Renal failure, comorbidity and mortality in preterm infants. Wien Klin Wochenschr 2008;120:153-7.
Doronjski A, Stojanovic V, Spasojevic S, Kovacevic B, Pavlovic V, Nikolic M, et al.
Acute renal failure in premature neonates. Vojnosanit Pregl 2009;66:863-7.
Gharehbaghi MM, Peirovifar A. Evaluating causes of acute renal failure in newborn infants. Pak J Med Sci 2007;23:877-80.
Mehta P, Sinha A, Sami A, Hari P, Kalaivani M, Gulati A, et al.
Incidence of acute kidney injury in hospitalized children. Indian Pediatr 2012;49:537-42.
Vasudevan A, Phadke KD. Acute kidney injury in children, look for it and don't ignore it! Indian Pediatr 2012;49:524-5.
Sutherland SM, Ji J, Sheikhi FH, Widen E, Tian L, Alexander SR, et al.
AKI in hospitalized children: Epidemiology and clinical associations in a national cohort. Clin J Am Soc Nephrol 2013;8:1661-9.
Spitzer A. Renal physiology and functional development. In: Edelmann CM, editor. Pediatric Kidney Disease. Boston: Little Brown; 1978. p. 25.
Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, et al.
Acute Kidney Injury Network: Report of an initiative to improve outcomes in acute kidney injury. Crit Care 2007;11:R31.
Alaro D, Bashir A, Musoke R, Wanaiana L. Prevalence and outcomes of acute kidney injury in term neonates with perinatal asphyxia. Afr Health Sci 2014;14:682-8.
Amardiyanto R, Pudjiastuti P, Rundjan L, Pushponegoro HD. Acute kidney injury in asphyxiated neonates. Paediatr Indones 2013;53:232-8.
Bhantnagar A, Bairwa AL, Meena KC. Incidence of KI in perinatal asphyxia and its correlation with HIE staging. Indian J Res 2014;3:12-3.
Gopal G. AKI in perinatal asphyxia. Indian J Pharm Biol Res 2014;2:60-5.
Venkataraman R, Kellum JA. Defining acute renal failure: The RIFLE criteria. J Intensive Care Med 2007;22:187-93.
[Table 1], [Table 2], [Table 3], [Table 4]