Asphyxia remains a common problem in the neonatal nursery and is a significant cause of morbidity and death in the term and preterm neonate. The incidence of asphyxia is estimated to be between 1 and 10 per 1000 live births and is influenced by the local availability of medical resources. Asphyxia can lead to multi-organ dysfunction and a redistribution of cardiac output to maintain cerebral, cardiac, and adrenal perfusion while potentially compromising renal, gastrointestinal, and skin perfusion.
When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/3622

Loboda, Andrii Mykolaiovych

Tabansi, V.

Лобода, Андрей Николаевич

Лобода, Андрій Миколайович

SocioEconomic Challenges Journal (Sumy State University)

  
 
 
INTERLEUKIN-18 AS A MARKER OF ACUTE KIDNEY INJURY IN ASPHYXIA OF 
NEONATES 
Loboda A., Tabansi V. 
Sumy State University, Department of Pediatrics with Medical Genetics 
 
Asphyxia remains a common problem in the neonatal nursery and is a significant cause of morbidity 
and death in the term and preterm neonate. The incidence of asphyxia is estimated to be between 1 and 10 
per 1000 live births and is influenced by the local availability of medical resources. Asphyxia can lead to 
multi-organ dysfunction and a redistribution of cardiac output to maintain cerebral, cardiac, and adrenal 
perfusion while potentially compromising renal, gastrointestinal, and skin perfusion. 
Acute kidney injury (AKI) is a common consequence of perinatal asphyxia, occurring in up to 56% of 
infants. A major difficulty in diagnosing this condition is the lack of a consensus definition of neonatal 
AKI, largely because of a dearth of specific measurable variables and biochemical markers. As markers 
of AKI may be used such substances as: NGAL (Neutrophil Gelatinase- Associated Lipocalcin), KIM-1 
9Kidney Injury Molecule 1), Cystatin C, NHE3 (Sodium-Hydrogen Exchanger, isoform 3), Interleukin-
18 etc. 
Interleukin-18 (IL-18, also known as interferon-gamma inducing factor) is a protein which in humans 
is encoded by the IL-18 gene.
 
IL-18 is a cytokine that belongs to the IL-1 super family and is produced by 
macrophages and other cells. Also IL-18 is synthesized by the proximal renal tubular epithelium under 
the influence of ischemic or nephrotoxic factors. Determine its level in urine allows at an early stage to 
determine the presence of renal tissue damage. 
This work will be given to the investigation of potential biomarker that may aid the clinician in the 
diagnosis of renal injury in this population. 
The main aim of the work is to demonstrate the importance of IL-18 as a marker of kidney 
injury/damage as a result of asphyxia in newborns. 
The study involved 100 full-term newborns with disturbance kidney function. Among them 50 
children had severe asphyxia and 50 had moderate asphyxia. Comparison group included 20 healthy 
newborns. The actual material used for the tests were urine samples from the neonates, that’s why 
laboratory method was non-invasive. The level of IL-18 in urine was determined on 1–2, 7–8 and 25–30 
days of life by ELISA. 
In neonates with impaired kidney function due to asphyxia the contents of IL-18 in urine during the 
neonatal period exceeded the concentration of healthy children. At 1–2 days of life the content of IL-18 in 
the urine was almost 4,5 times higher (14.56 ± 0.83 pg/ml, p <0.05) in the case of moderate asphyxia and 
9 times higher (30.55 ± 2.62 pg/ml, p <0.05) in the case of severe asphyxia. Thus, urine IL-18 may be an 
early predictor of renal dysfunction in infants who are exposed to asphyxia. High content of IL-18 in the 
urine of children with severe asphyxia indicates significant damage to the epithelium of the proximal 
renal tubules. 
Further dynamics of IL-18 in the urine was similar in both groups of children with asphyxia. Cytokine 
content declined by one-third to the end of the first week of life (9.75 ± 0.19 pg/ml and 21.65 ± 2.38 
pg/ml in newborns with moderate and severe asphyxia respectively), but remained statistically higher 
than the comparison group. Thus the difference between the groups of neonates with asphyxia was still 
present, indicating the dependence of renal tubular injury from the severity of asphyxia. 
In the late neonatal period cytokine levels were equal in the examined groups of children with 
asphyxia and more than 3.5 times higher (p <0.05) than the content in the comparison group. So, after 
asphyxia tubular dysfunction persists long enough, requiring a prolonged monitoring the renal function in 
this category of infants. 
Conclusion. Level of IL-18 in the urine in the first 24–48 hours of life is an early diagnostic sign of 
kidney damage in newborns with asphyxia. After asphyxia tubular dysfunction persists long enough. This 
is evidenced by the high content of IL-18 in the urine during whole neonatal period. 
 
 
 
 
 
Актуальні питання теоретичної та практичної медицини : збірник тез доповідей ІІ Міжнародної 
науково-практичної конференції студентів та молодих вчених, м. Суми, 16-18 квітня 2014 р. / М.В. 
Погорєлов. - Суми : СумДУ, 2014. - С. 227. 


English

Interleukin-18 as a marker of acute kidney injury in asphyxia of neonates

Electronic Sumy State University Institutional Repository

    INTERLEUKIN-18 AS A MARKER OF ACUTE KIDNEY INJURY IN ASPHYXIA OF NEONATES Loboda A., Tabansi V. Sumy State University, Department of Pediatrics with Medical Genetics  Asphyxia remains a common problem in the neonatal nursery and is a significant cause of morbidity and death in the term and preterm neonate. The incidence of asphyxia is estimated to be between 1 and 10 per 1000 live births and is influenced by the local availability of medical resources. Asphyxia can lead to multi-organ dysfunction and a redistribution of cardiac output to maintain cerebral, cardiac, and adrenal perfusion while potentially compromising renal, gastrointestinal, and skin perfusion. Acute kidney injury (AKI) is a common consequence of perinatal asphyxia, occurring in up to 56% of infants. A major difficulty in diagnosing this condition is the lack of a consensus definition of neonatal AKI, largely because of a dearth of specific measurable variables and biochemical markers. As markers of AKI may be used such substances as: NGAL (Neutrophil Gelatinase- Associated Lipocalcin), KIM-1 9Kidney Injury Molecule 1), Cystatin C, NHE3 (Sodium-Hydrogen Exchanger, isoform 3), Interleukin-18 etc. Interleukin-18 (IL-18, also known as interferon-gamma inducing factor) is a protein which in humans is encoded by the IL-18 gene. IL-18 is a cytokine that belongs to the IL-1 super family and is produced by macrophages and other cells. Also IL-18 is synthesized by the proximal renal tubular epithelium under the influence of ischemic or nephrotoxic factors. Determine its level in urine allows at an early stage to determine the presence of renal tissue damage. This work will be given to the investigation of potential biomarker that may aid the clinician in the diagnosis of renal injury in this population. The main aim of the work is to demonstrate the importance of IL-18 as a marker of kidney injury/damage as a result of asphyxia in newborns. The study involved 100 full-term newborns with disturbance kidney function. Among them 50 children had severe asphyxia and 50 had moderate asphyxia. Comparison group included 20 healthy newborns. The actual material used for the tests were urine samples from the neonates, that’s why laboratory method was non-invasive. The level of IL-18 in urine was determined on 1–2, 7–8 and 25–30 days of life by ELISA. In neonates with impaired kidney function due to asphyxia the contents of IL-18 in urine during the neonatal period exceeded the concentration of healthy children. At 1–2 days of life the content of IL-18 in the urine was almost 4,5 times higher (14.56 ± 0.83 pg/ml, p <0.05) in the case of moderate asphyxia and 9 times higher (30.55 ± 2.62 pg/ml, p <0.05) in the case of severe asphyxia. Thus, urine IL-18 may be an early predictor of renal dysfunction in infants who are exposed to asphyxia. High content of IL-18 in the urine of children with severe asphyxia indicates significant damage to the epithelium of the proximal renal tubules. Further dynamics of IL-18 in the urine was similar in both groups of children with asphyxia. Cytokine content declined by one-third to the end of the first week of life (9.75 ± 0.19 pg/ml and 21.65 ± 2.38 pg/ml in newborns with moderate and severe asphyxia respectively), but remained statistically higher than the comparison group. Thus the difference between the groups of neonates with asphyxia was still present, indicating the dependence of renal tubular injury from the severity of asphyxia. In the late neonatal period cytokine levels were equal in the examined groups of children with asphyxia and more than 3.5 times higher (p <0.05) than the content in the comparison group. So, after asphyxia tubular dysfunction persists long enough, requiring a prolonged monitoring the renal function in this category of infants. Conclusion. Level of IL-18 in the urine in the first 24–48 hours of life is an early diagnostic sign of kidney damage in newborns with asphyxia. After asphyxia tubular dysfunction persists long enough. This is evidenced by the high content of IL-18 in the urine during whole neonatal period.      Актуальні питання теоретичної та практичної медицини : збірник тез доповідей ІІ Міжнародної науково-практичної конференції студентів та молодих вчених, м. Суми, 16-18 квітня 2014 р. / М.В. Погорєлов. - Суми : СумДУ, 2014. - С. 227. 

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Interleukin-18 as a marker of acute kidney injury in asphyxia of neonates

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