The evidence for ethnic or racial influence on CKD is mainly epidemiological. The incidence of kidney failure requiring dialysis is higher in a wide variety of non-white groups (African-American, Asian, Native American, Native Australian, and Pacific Islander) than in white groups of European heritage in North America, Europe, and the Hypertension is also more common, develops earlier in life, and manifests with a higher average BP among African-Americans than whites in the Although profound environmental and socioeconomic issues are clearly involved, information is gradually being gathered that enlightens us about some of the links among genetics, high BP and kidney disease in the African-American Genetic variance in the non-muscle myosin heavy chain 9 gene (MYH9) was reported to be partly responsible for progressive kidney disease in hypertensive This might provide a rationale for lower BP targets in hypertensive African-Americans than other racial groups,439 especially in African-Americans with genetic variation in the MYH9 gene. More recently, polymorphisms in the apolipoprotein L-1 gene (APOL1), which is located immediately upstream to MYH9, has been implicated in this process, with the APOLI G1 and G2 alleles associating with focal segmental glomerulosclerosis in Intriguingly, these variants seem to confer resistance to Trypanosoma brucei rhodesiense, which may explain the persistence of this seemingly otherwise disadvantageous gene in West Africans, but this hypothesis does not clarify the association between APOL1 and focal segmental glomerulosclerosis. Epidemiological evidence is suggestive of many other ethnic racial differences among individuals with CKD. In addition to the differences in the prevalence of types of kidney diseases in different groups, there appear to be differences in the rates of CKD progression, in the effects of BP control on CKD progression, in BP responses to various antihypertensive regimens, and in cardiovascular risk asso- ciated with a particular BP level. 