Abstract
Chronic kidney disease (CKD) disproportionately affects people of African ancestry worldwide including those living in Europe and the United States (US), with overrepresentation among those with advanced CKD and kidney failure. This excess burden reflects the convergence of genetic susceptibility, including Apolipoprotein-L1 (APOL1) risk variants and sickle-cell–related nephropathy, with early-life factors such as low birth weight, high rates of hypertension and diabetes, and recurrent acute kidney injury from infections or environmental exposures. Social and structural drivers including poverty, limited nephrology access, systemic racism, and medical mistrust may further accelerate disease progression.
Accurate diagnosis is hampered by historic reliance on race in estimating kidney function. The inclusion of a race coefficient in eGFR equations embeds a social label into a biological formula, delaying CKD recognition and treatment. Current guidance supports race-free equations and the selective use of ancestry-informed genetic tools, such as APOL1 testing, within ethical frameworks.
Management requires attention to both biology and context. Hypertension remains the leading modifiable risk factor but is often more severe and less well controlled; culturally tailored community programmes, including barbershop and church-based interventions, improve blood pressure and engagement. Glomerulonephritis, infections such as HIV, and heat- or toxin-related kidney injury remain major causes of CKD across Africa, compounded by scarce diagnostic capacity and low nephrologist density, and are likely to contribute to disease in Diaspora.This review outlines the global burden, key causes, diagnostic challenges, and socioeconomic and health-system barriers specific to African ancestry populations in Europe, and highlights precision strategies (genetic, clinical, and community-based) to promote equitable kidney care.