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Self-reported ethnicity reflects many sources of variation, including genetic. Biologic variation is associated with several population-specific risks for disease. There are several inherited factors associated with African American populations compared to European American, and these include differences in the risk for type 2 diabetes mellitus, non-diabetic nephropathy, kidney stones, atherosclerosis, and osteoporosis. Treatment responses to interferon therapy for hepatitis C also depend on interferon-lambda3 (IL28B) genotypes, which differ markedly across population groups and partially explain ethnic specific response rates. Dr. Freedman will discuss these topics as well as review Regional Admixture Mapping (RAM) and Mapping by Admixture Linkage Disequilibrium (MALD) for detecting genetic associations in admixed populations.
Of particular scientific interest, non-diabetic nephropathy susceptibility in African Americans is dependent on variation in the apolipoprotein L1 gene (APOL1). Coding APOL1 risk variants protect from African sleeping sickness. Risk variants are virtually absent in European-derived populations, but 12 percent of African Americans possess two risk variants. APOL1-associated nephropathy encompasses up to 40 percent of all end-stage renal disease (ESRD) in African Americans, including HIV-associated nephropathy, idiopathic focal segmental glomerulosclerosis, "hypertension-attributed nephropathy," sickle cell nephropathy, and ESRD associated with lupus nephritis. Second hits, such as genes or environmental factors, appear to be required for nephropathy initiation. This finding alters the epidemiology of ESRD in African Americans; that is, hypertension is not a common cause of nephropathy. Thus, understanding the genetic basis of ethnic differences in disease will clarify the roles of environmental exposures on risk and lead to development of novel treatments.
Author:
Barry Freedman, M.D., Wake Forest School of Medicine
