Chronic kidney disease is regarded as a major global public health concern, and the problem is most acute in black people. This has been attributed to what is common in African-origin genes that have a big bearing on kidney disease risk factors. These genetic differences, especially in the APOL1 gene, predispose people to develop worse forms of kidney disease, such as focal segmental glomerulosclerosis (FSGS) and hypertension-attributed end-stage kidney disease (H-ESKD), due to high blood pressure. Recent studies have cast some light on how these same variants, which seemingly provide immunity to African sleeping sickness, regrettably are partly responsible for kidney disease that is endemic in the African and African-American communities. Genetic factors eliciting kidney disease in such population groups must be understood to enable proper formulation of intervention and, additionally, the care strategies and treatments aimed at improving health disparities that affect such communities.
APOL1 Variants and Kidney Disease Risk
The association of the APOL1 gene to chromosome 22 codes for apolipoprotein L-1, which is a protein functional for breaking down trypanosomes, the causative agent for African sleeping sickness. There are two renal risk variants of the APOL1 gene, the G1 and G2, which are prevalent among the African population. They seem to have been shaped by this antitrypanosomal effect against Trypanosoma brucei, a trypanosome species that is endemic to sub-Saharan Africa. However, persons who possess these variants are much more susceptible to FSGS and H-ESKD – both ailments that can result in kidney failure. Research shows these variations are linked with a 10.5 risk of FSGS and a 7.3 risk of H-ESKD among African Americans.