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Updated: Dec 24, 2025

Use of Ultra-high Field MRI in Small Rodent Models of Polycystic Kidney Disease for In Vivo Phenotyping and Drug Monitoring
Published on: June 23, 2015
A focus on the association of Apol1 with kidney disease in children
Pepe M Ekulu1,2, Agathe B Nkoy3, Oyindamola C Adebayo4
1Department of Development and Regeneration, KU Leuven, Leuven, Belgium. drmfutu@yahoo.fr.
Insights
Individuals of African origin with APOL1 risk variants face higher risks for progressive chronic kidney diseases (CKD). This review examines APOL1
Area of Science:
- Nephrology
- Genetics
- Immunology
Background:
- Individuals of African origin exhibit a higher predisposition to progressive chronic kidney diseases (CKD).
- Genetic variants (G1, G2) in the apolipoprotein-L1 (APOL1) gene are implicated in this increased CKD risk.
- APOL1 risk variants are linked to hypertension, albuminuria, and accelerated kidney function decline in pediatric populations, particularly those with sickle cell disease (SCD) or HIV.
Purpose of the Study:
- To review existing epidemiological data on APOL1-related CKD in children.
- To explore racial disparities in CKD.
- To examine the role of APOL1 in innate immunity and pathogenic pathways of kidney injury.
Main Methods:
- Literature review of epidemiological studies on APOL1 and pediatric CKD.
- Analysis of data on racial disparities in CKD prevalence.
- Synthesis of research on APOL1's role in immunity and kidney injury mechanisms.
Main Results:
- APOL1 risk variants are significantly associated with CKD development and progression in children.
- Racial disparities in CKD are partly explained by APOL1 genetic factors.
- APOL1 influences innate immunity and contributes to kidney damage through specific pathogenic pathways.
Conclusions:
- APOL1 genetic variants are a critical factor in the increased risk and progression of CKD among individuals of African origin, including children.
- Understanding APOL1's role is crucial for addressing racial disparities in pediatric CKD.
- Further research into APOL1-mediated pathogenic pathways may reveal novel therapeutic targets for kidney disease.
Abstract:
Individuals of African origin have an increased risk of developing various progressive chronic kidney diseases (CKD). This risk has been attributed to genetic variants (G1, G2) in apolipoprotein-L1 (APOL1) gene. In the pediatric population, especially in children affected by sickle cell disease (SCD), by human immunodeficiency virus (HIV), or with various glomerular diseases, APOL1 risk variants have been associated with the development of hypertension, albuminuria, and more rapid decline of kidney function. The present review focuses on existing APOL1-related epidemiological data in children with CKD. It also includes data from studies addressing racial disparities in CKD, the APOL1-related innate immunity, and the relationship between APOL1 and CKD and pathogenic pathways mediating APOL1-related kidney injury.
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