RENAL DERANGEMENT IN NEONATES WITH ASPHYXIA
NEONATORUM­­

1.           ABSTRACT

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Introduction: Severe hypoxic ischemic organ damage is caused by asphyxia in
newborns which can follow fatal outcomes or severe life-long pathologies like
renal insufficiency. We wanted to note the frequency of renal derangement in
neonates having asphyxia neonatoum in this study.

Setting: Department of Pediatrics, Bahawal Victoria Hospital (BVH), Bahawalpur,
from 1st January 2017 to 31st June 2017.

Materials & Methods: Two
hundred and sixty four neonates of both genders with birth asphyxia were
included in the study. Main outcome was
renal derangement in asphyxia neonatorum.

Results: Mean weight was 2.54 kg with
standard deviation 0.50 kg and having mean APGAR score 4.43 with SD 1.66. It was noted that 189 (71.6%) neonates had Renal
derangement in which
109 (57.7%) were males and 80 (42.3%) were females with mean of weight was
2.53kg, having mean APGAR score 4.44.

Conclusion: Renal derangement is quite common in neonates with
birth
asphyxia.

Keywords: Asphyxia Neonatorum, Renal Derangement, Apgar score, Low Birth
Weight.

 

 

INTRODUCTION:

Perinatal asphyxia is a significant
factor contributing to neonatal morbidity and mortality around the world.1
Global incidence of Perinatal asphyxia is 1.0-1.5%.2 WHO
reports that ~1 million children die worldwide annually with birth asphyxia. Distinguish between mild and severe
asphyxia is a difficult task. Improving diagnosis and early prediction of asphyxiated
neonates has been in focus for researchers in the recent years.3

Asphyxia damages the CNS, leading to CNS related complications.
Asphyxia is caused by oxidative stress, raised cerebral permeability, birth
trauma and metabolic complications.4 Measuring oxidative stress
markers can predict outcomes in newborns with asphyxia.5 Acute
kidney injury is associated with perinatal asphyxia, responsible for about 50%
of cases.6 The pathology of specific biomarkers has been of huge clinical
value in the recent years.7 Renal
insufficiency is more frequent within 24 hours of a hypoxic ischemic episode.8
Early detection of renal failure aid to appropriate fluid and electrolyte
management. Diagnosing renal failure is challenging as some of the established
clinical and biochemical parameters are untrustworthy.9 In newly
born, S100B has been found to be significantly
increased in blood serum when noted after 24 hours of severe birth asphyx
insult.10,11

Gupta BD conducted a study on neonates having asphyxia and renal failure, found that 78% of axphyxiated
neonates had nonoliguric renal failure12
while oliguric failure was seen in 21%. We conducted this study to note the frequency of renal derangement in
neonates with asphyxia neonatoum.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

MATERIAL
AND METHODS:

This was a descriptive
study conducted in department of pediatrics, Bahawal Victoria Hospital (BVH), Bahawalpur,
from 1st January 2017 to
31st June 2017. A total of 264 term neonates of both gender,
having asphyxia, delivered in gynecology department of BVH, Bahawalpur, were
included in this study with non probability consecutive sampling technique. Newborns
with renal
insufficiency or oligohydrominas seen by antenatal ultrasound, or having
history of maternal addiction of analgesia and severe infection were excluded
from the study.

Ethical
committee of BVH approved the study. Informed consent was taken from the
guardians/parents of the newborns and confidentiality of the data and identity
was ensured. Blood sample for serum creatinin were taken at 72 hours of life.
Risks/benefits of this study and protocols were discussed with parents/guardians.
Weight of the newborns was noted at the time of birth.

Mean and
standard deviation were noted for quantitative variables like APGAR score and birth
weight. Frequency and percentages were calculated for qualitative variables like
gender and renal derangement. Stratification was done to control the effect
modifier like birth weight, APGAR score and gender. Chi square test was applied
and a p value ? 0.05 was considered statistically significant.

 

 

RESULTS:

Total neonates included in this
study were 264 (100%) having mean of weight was 2.54 kg with standard deviation
was 0.50 and having mean of APGAR score was 4.43 with SD 1.66. Out of 264
neonates it was observed that 147(55.7%) were males with mean weight was 2.59 kg and
standard deviation was 0.493 And 117(44.3%) were females with mean weight was 2.47 kg
and standard deviation was 0.501.

Out of 264 neonates, it was noted
that 189 (71.6%) neonates suffered from Renal derangement in which
109 (57.7%) were males and 80 (42.3%) were females with mean of weight was
2.53kg and standard deviation was 0.5 and having mean of APGAR score was 4.44
with standard deviation was 1.667. It was also observed that 75 (28.4%)
neonates were not suffered from Renal derangement in which 38
(50.7%) were males and 37 (49.3%) were females with mean of weight 2.56 kg and
standard deviation was 0.5 and having mean of APGAR score was 4.40 with
standard deviation was 1.652.

When stratified analysis was done
to see the effect modification it was noted that there was no significant
effect of renal derangement on birth weight (?2.5 kg and >2.5
kg) and gender having p values 0.650 and 0.301 respectively. But significant association
of APGAR score with renal derangement was seen with p value 0.0001

 

  

 

DISCUSSION:

Adaptive mechanism is responsible
for renal injury in asphyxiated newborns. Acute tubular necrosis, renal vein
thrombosis and renal failure occur commonly and the prognosis is poor that has
been documented to cause irreversible renal damage in ~40% of the survivors.8 Urinary output is slightly
less in neonates with severe birth asphyxia but with statistical insignificance
in comparison to mild and moderate degree of asphyxia. Oliguria has been accounted
in higher numbers from 25-69%.9,10
Mixed response of individual nephron and variable damage to tubular epithelium may
end up causing anatomical damage, then further leading to reduction in single
nephron GFR, so, declining tubular fluid flow.11

About 10% of neonates develop
hematuria and end up presenting with urinary red cell count up to 10 cells/mL.12
Abnormal tubular function post asphyxia may lead lead to significant tubular
proteinuria. Qualitative assessment of proteinuria has been proposed by
measuring p2-M-a low molecular weight protein to detect tubular injury.13,14 The mechanism of increased levels of urea and creatinin
have been hypothesized as a result of obstructed tubular lumen and back leak
mechanism. 15

The incidence of renal involvement
observed in the current study was 47% that is consistent with earlier findings.15-17 Sonographic
abnormalities were seen along with biochemical verification of renal
dysfunction and three neonates were oliguric. Out of a total of 5 neonates with
abnormal sonography, 4 died. None of the neonate was oliguric by 4th
to 6th day of life which. This finding was pretty comparable to what
Pertman, et al found.8
Decrease in number of functional nephrons leads to ARF, evokes compensatory
hypertrophy of the residual nephrons. This can proceed to better renal
functions in early months of life.  

It has been reported earlier that
40% of survivors had decreased creatinin clearance, renal tubular acidosis or
concentrating defect.18
Oliguria, abnormal renal sonographic scan and hyponatermia were revealed as the
most important signs predicting mortality in our study.

 

 

 

 

 

 

 

 

 

 

CONCLUSION:

Renal derangement is quite frequent
in asphyxiated neonates mostly with nonoliguric failure. Extent of renal dysfunction
is directly related to degree of asphyxia.

 

REFERENCES:

1.     Volpe
JJ. Hypoxic ischemic encephalopathy. In: Volpe JJ. Ed. Neurology of newborn. 4th
edition Philedelphia:WB Saunders;2001:217-394.

2.     Aurora
S,Synder E Y, Perinatal asphyxia .In Cloherty J P.Manual of neonatal care .4th
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3.     Peeva V,
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4.     Shah S, Goel AK, Padhy M, Bhoi S.
Correlation of oxidative stress biomarker and serum marker of brain injury in
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5.     Mondal N, Bhat BV,
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6.     Coulibaly G,
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Perinatal asphyxia and acute renal insufficiency in Quagadougou. Arch Pediatr.
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7.     DurkanAM, Alexander
RT. Acute kidney injury post neonatal asphyxia. J Pediatr. 2011;158:29–33.

8.     Perlman JM, Tack ED, Martin T,
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9.     Misra PK, Kumar A, Natu SM, Kapoor
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10.           
 Murabayashi M, Minato M, Okuhata Y, Makimoto M, Hosono S, Masaoka N, et
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11.           
Florio P, Abella R, Marinoni E, Di Iorio R, Li Volti G,
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(Schol Ed). 2010;1:47–72.

12.           
Gupta BD. Renal failure asphyxiated neonates. Indian
Pediatr. 2005 sep;42(9):928-34.

13.           
Ferriero DM. Neonatal brain injury. N Engl J Med. 2004 Nov 4.
351(19):1985-95. 

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2002 Dec. 29(4):585-602. 

16.           
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17.           
Stola A, Perlman J. Post-resuscitation strategies to avoid
ongoing injury following intrapartum hypoxia-ischemia. Semin Fetal Neonatal Med.
2008 Dec. 13(6):424-31. 

18.           
Laptook A, Tyson J, Shankaran S. Elevated temperature after
hypoxic-ischemic encephalopathy: risk factor for adverse outcomes. Pediatrics. 2008 Sep.
122(3):491-9.