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Published on: June 30, 2018
Assessment of Renal Function Status in Steady-State Sickle Cell Anaemic Children Using Urine Human Neutrophil
Olatubosun Oladipupo Olawale1, Abiodun Folasade Adekanmbi2, Ayobola Abimbola Sonuga3
1Department of Chemical Pathology and Immunology, Olabisi Onabanjo University Teaching Hospital, Sagamu, Nigeria.
Insights
Children with sickle cell anaemia show early signs of kidney damage, indicated by higher urine albumin-to-creatinine ratio (ACR). Urine NGAL and NCR were not sensitive markers in this young population due to hyperfiltration.
Area of Science:
- Nephrology
- Pediatrics
- Hematology
Background:
- Sickle cell anaemia (SCA) involves defective hemoglobin synthesis, leading to endocrine and metabolic issues.
- Kidney function alterations in SCA are multifactorial and can manifest early in childhood.
Purpose of the Study:
- To assess renal function in children with SCA using urine albumin-to-creatinine ratio (ACR) and urine human neutrophil gelatinase-associated lipocalin (NGAL).
Main Methods:
- A case-control study involving 200 children (5-15 years) in Nigeria (150 SCA, 50 controls).
- Assayed serum urea, creatinine, urine albumin, and NGAL.
- Calculated estimated glomerular filtration rate (eGFR), urine ACR, and urine NGAL/creatinine ratio (NCR).
Main Results:
- SCA children had significantly lower weight, height, BMI, blood pressure, urea, and creatinine compared to controls.
- SCA children exhibited significantly higher eGFR, urine albumin, and urine ACR.
- No significant difference in urine NGAL and NCR between groups, though levels were higher in SCA children.
Conclusions:
- Elevated urine ACR in SCA children suggests early-onset kidney injury.
- Urine NGAL and NCR may not be sensitive markers for kidney disease in young SCA patients due to hyperfiltration.
Introduction:
Sickle cell anaemia is characterized by defective haemoglobin synthesis and is associated with both endocrine and metabolic alterations. The effects of this clinical condition on kidney function are multifactorial and often begin early in childhood. This study aims to assess renal function in children with sickle cell anaemia using urine albumin:creatinine ratio (ACR) and urine human neutrophil gelatinase-associated lipocalin (NGAL).
Methods:
This case-control study was conducted on 200 children aged 5-15 years in 2 tertiary hospitals in South West Nigeria: 150 were of haemoglobin S genotype and 50 were of haemoglobin A genotype. Serum urea, creatinine, urine albumin, and NGAL were assayed by known standard methods. eGFR, urine ACR, and urine NGAL/creatinine ratio (urine NCR) were calculated.
Results:
The weight, height, BMI, systolic blood pressure, plasma urea, plasma creatinine, and spot urine creatinine of the HbS genotype children were significantly lower compared to that of the HbA genotype children. The eGFR, spot urine albumin, and urine ACR were significantly higher in the HbS group compared to the HbA group. There was no significant difference in the spot urine NGAL and urine NCR between the 2 groups, though both were higher in the HbS group compared to the HbA group.
Conclusions:
Kidney injury probably starts early in childhood in sickle cell individuals as indicated by the higher urine ACR detected in them. We infer that urine NGAL and uNCR are not sensitive markers of kidney disease especially in young sickle cell individuals possibly because of the hyperfiltration present at this age.
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