Does low income have any bearing on the degree of proteinuria, and if so, does it have racial differences? A cross-sectional study published in American Journal of Kidney Diseases explores this question in more detail. Dr. Deidra Crews (DC), corresponding author from Johns Hopkins School of Medicine, discusses the recent manuscript with Dr. Joel Topf (eAJKD), eAJKD Advisory Board member.
eAJKD: How did you develop interest in studying racial disparities in kidney diseases?
DC: My research focus is on the interplay of socioeconomic and racial disparities. My mentor and co-author on this study Dr. Neil Powe was my inspiration. He has had a long and distinguished career focused on racial disparities in kidney disease. Also, I am African American and have some family members with kidney disease. This has become my passion.
eAJKD: Where does this particular study about income disparities and race fit into the full narrative of racial disparities in kidney diseases?
DC: Our work in this field was initiated with a Baltimore-based cohort called HANDLS, the Healthy Aging, and Neighborhoods of Diversity across the Life Span. It’s a cohort of black and white adults who were sampled across a range of incomes. The concept behind the cohort was to try to tease out whether race or socioeconomic status was responsible for disparities seen in some of the conditions that become prevalent as people aged. In the initial studies, we found that low-income was more strongly associated with chronic kidney disease (CKD) among blacks than it was among whites. That was a small cohort of participants. The findings needed to be replicated with larger numbers of participants so we can get a good range of income status and better understand these relationships.
eAJKD: What is the biologic plausibility that income and race could interact to increase albuminuria?
DC: One possibility would be the influence on health behaviors. If you’re a low-income African American (AA), chances are you live in a fairly racially segregated neighborhood where access to full-service grocery stores may be limited, or fast food restaurants appear on every corner. Processed foods and less access to foods that we tend to think of as being associated with better cardiovascular and renal health may contribute to this finding.
Cultural differences in dietary habits may be in play as well. If you’re a poor AA, you may use your limited resources to purchase foods that are different from what a poor Caucasian person may purchase.
Environment is another major factor. If you’re a poor AA, you may live in an area where there’s not a lot of access to parks or places where there are sidewalks for you to take part in recreation.
The psychological stress of poverty may be different for AA and they might induce more endothelial damage. There have been some studies that link decreased heart rate variability to race. A few studies have shown that blacks tend to have their heart rates rise during increased stress levels, and not return to baseline soon thereafter. That has been linked to endothelial injury. There are a number of potential pathways between the stressors, poverty, and albuminuria that could exist.
eAJKD: How do these socioeconomic factors influence what we are learning about genetic predisposition with APOL1? Does the gene distribute evenly across socioeconomic terrain, or does it cluster with economic strata?
DC: I think that is something we need to investigate further. One question would be if AA individuals with this polymorphism and lower income are more likely to have manifestation of proteinuric kidney disease? That hasn’t been looked at yet, but I would suggest again that there is some key gene-environment interaction taking place. Perhaps poverty is the second hit.
eAJKD: In all of your models, there was a race-socioeconomic association among whites that persisted until you got to the multi-varied analysis before it disappeared. You further state that this actually strengthens your underlying hypothesis that there is something specific about being AA that results in kidney disease.
DC: Our overarching hypothesis is that there’s something different about being poor for AA.
eAJKD: But different for poverty in AA?
DC: I think the experience of poverty is different for AA than it is for whites. That’s the reason why we can’t adjust away the differences by accounting for confounders. There is an excess of kidney disease in poor white people. We assume that is from obesity and diabetes. Once we adjust for diabetes and obesity, that association disappears. We’re not seeing that when we do that for the black participants. That leads to the argument that there’s something different, un-adjustable, in terms of what it means to be poor and AA.
eAJKD: Is it possible that the kidney disease causes the poverty, rather than the poverty causing the kidney disease?
DC: I think it is improbable at this degree of kidney function. If we were doing a study among end-stage renal disease patients where we know that the burden of disability is quite high, then I think that that idea would be more valid. But I think among this relatively healthy cohort it’s less likely.
eAJKD: Perhaps the people with albuminuria may have parents with more debilitating kidney disease, and that they were then brought up in a poor family because a parent was on dialysis?
DC: I think that would be unusual. End-stage renal disease is rare. It would be rare for this population of 25,000 people to have a substantial proportion of them raised in a family where someone had advanced kidney disease.
eAJKD: What study design should we demand to really give us the best picture of this situation?
DC: I think looking at the gene-environment interaction would be important. Some of these growing cohort studies have APOL1 information for a number of participants. Looking at the relationship between some socioeconomic factors and APOL1 and the risk of developing kidney disease is an important area of investigation.