Our main finding is that race and family income were independently associated with GFR level and this effect was similar for whites and blacks in our study. In contrast, neighborhood poverty was not associated with GFR. Further, accounting for household and community poverty attenuated some, but not all, of the unexpectedly higher prevalence of CKD among whites compared to blacks. These observations suggest that (1) household poverty increases the likelihood that both black and whites will have more severe reductions in GFR; (2) this effect of poverty is comparable or greater among whites, and (3) poverty as measured in our study cannot fully explain racial disparities in the prevalence of early stages of CKD in the this population.
The increased prevalence of CKD (GFR <60 ml/min/1.73 m2
) among whites compared to blacks was first identified in the National Health and Nutrition III (NHANES) Study [12
] and previously reported for the REGARDS cohort [14
]. Even after including the presence of proteinuria as well as a GFR of <60 ml/min/1.73 m2
in the definition of CKD, analysis of later NHANES surveys conducted between 1999 and 2004, found the prevalence of all stages of CKD to be 16.1% (95% CI 16.6–18.7%) among whites and 19.9% (95% CI 18.2–21.8%) among blacks [22
], clearly unexpected in view of the fourfold increased incidence of ESRD among blacks consistently reported for the US population. Of note, the 30% increased prevalence among blacks reflected an increased prevalence of persistent albuminuria among individuals with a GFR of ≥60 ml/min/1.73 m2
and, as with earlier NHANES reports, the prevalence for whites and blacks of a GFR between 30 and 59 ml/min/1.73 m2
was 5.8 and 4.7% and of a GFR between 15 and 29 ml/min/1.73 m2
, 0.3 and 1.1% [22
It has been suggested that blacks may experience more rapid progression to ESRD, thus contributing to higher incidence rates but not the prevalence of lower GFR. Factors that might mediate more rapid progression may include genetic susceptibility to kidney injury like the recently reported polymorphisms in the nonmuscle myosin heavy chain-9 (MYH9) gene which are associated with increased risk of ESRD among blacks [23
], environmental exposures, and barriers to healthcare [24
]. Another possible contributing factor is that differential survival among individuals with CKD might contribute to these racial disparities [26
There is growing interest in the role of SES as a modifying influence on racial disparities in the risk of progressive kidney disease and ESRD [27
]. Risk factors associated with poverty that might accelerate the progression of CKD associated with SES include perinatal factors and low birth weight, behavioral exposures like smoking, analgesic and other drug use, lead exposure due to illicit alcohol or pica consumption, and access and adequacy of healthcare. It is possible that poverty-related exposures might interact with genetic factors predisposing to rapid loss of kidney function or increased mortality rates among individuals with lower GFR and thus contribute to racial disparities in the prevalence of CKD.
There is increasing evidence to support a role of poverty and SES in a more rapid decline in GFR. Peralta et al. [29
] used a genetic admixture score based on 24 genetic markers to estimate the degree of African ancestry in the Cardiovascular Health Study, and found that the degree of African ancestry was not associated with either baseline or change in kidney function. Decreasing income, in contrast, was associated with an increased prevalence of impaired kidney function and this association persisted after controlling for African ancestry, age, gender, smoking status, diabetes, hypertension, education and occupation. The ARIC cohort study found increasing neighborhood poverty was associated with an increased 9-year risk of a composite outcome measured by an increase in serum creatinine level of 0.4 mg/dl or more, hospitalization for CKD, or death [15
]. A decreasing neighborhood SES score was associated with higher age-adjusted incidence rates among white males but not other race-gender groups.
These observations were repeated for elderly white participants in the Cardiovascular Health Study [30
] where the age-adjusted incidence rate for a composite outcome was 60% higher in the lowest versus the highest quartile of SES, and was unchanged after controlling for other covariates. Finally, a report using NHANES III data by Martins et al. [31
] found that blacks were 25% more likely than whites (OR 1.25, 95% CI 1.10, 1.43) to have a urinary albumin to creatinine ratio (ACR) between 30 and 300 mg/g and 80% more likely (OR 1.80, 95% CI 1.31, 2.49) to have an ACR in excess of 300 mg/g. When subjects were stratified into low and high poverty levels based on reported income, the black:white OR was lower, reflecting a diminished effect of race on prevalence of proteinuria, in the higher compared to lower poverty level [31
We recently reported that increasing census tract poverty level was strongly associated with a higher ESRD incidence for both blacks and whites [10
]. We found that, while the magnitude of the rate difference between black and white ESRD incidence rates increased, the black:white relative risk declined as community poverty increased. These opposite effects were due to a greater rate of rise in white compared to black ESRD incidence rates as community poverty increased, raising the possibility that the impact of lower socioeconomic conditions on ESRD risk may be greater in whites. Our current study is consistent with that possibility as controlling for the effect of lower personal income on racial disparities in the prevalence of decreased GFR reduced the impact of declining GFR on black:white prevalence differences, leaving the unresolved issue of why, despite a substantial fourfold increase in risk of all-cause ESRD among blacks, they are substantially less likely to have prevalent CKD.
It should be noted in this comparison that the majority of blacks live in census tracts with high community poverty. As the level of GFR declined the proportions with low household income increased tenfold in blacks and sevenfold in whites. Thus, larger proportions of black as compared to whites with more severe CKD have low family incomes. Previously reported racial disparities in incident ESRD associated with community poverty may reflect these population differences. However, we cannot reconcile these observations until we have accumulated sufficient follow-up time to examine the risks associated with personal income and community poverty in the REGARDS cohort.
A major strength of our study is that of a large, random sample of the older US population which provides sufficient numbers of cases to examine the full range of impaired kidney function below a GFR of 60 ml/min/ 1.73 m2
. It is unlikely that the racial differences in the prevalence of CKD we report are due to biased selection of subjects. Further, the possibility of misspecification of kidney function is reduced as we used an appropriately calibrated serum creatinine and the MDRD equation, which has been extensively validated for both whites and blacks, to estimate GFR [18
]. We only had complete information on 74.6% of our subjects and this raises a concern that the subjects included in our analyses may not be representative of our entire cohort leading to a biased assessment of association between individual and community SES measures and the distribution of kidney function blacks and whites. We have addressed this in several ways. First, when we included subjects with missing income information in our models using an indicator for poverty status that accounted for missing income our results were essentially unchanged (data not shown). Second, we compared the key attributes in our analyses (GFR, household income, and community poverty status) for the whole cohort, those included in our analyses and those who we excluded. Mean age, race, the proportions with low household incomes and living in poor communities, and the distribution of CKD are comparable for all subjects, those included in our analyses and those with one or more missing data element. In contrast, compared to men, women were more likely to have missing data. However, our main observation of an independent association between GFR and race that persists in sequential models controlling first for GFR, next for income, then community poverty, and finally demographic characteristics is consistent across models and we feel this reduces the likelihood of substantial selection bias. Thus, while we cannot exclude the possibility that the subjects excluded for our analyses may have altered our conclusions, we feel that the comparability of the excluded and included subjects and the consistency of our crude and adjusted results lessens this possibility.
A weakness of our study is that our measure of household income is by self-report and was not validated, and previous studies suggest that considerable misclassification of income status may occur with self-reported income data [30
], although the misclassification and failure to report seems to be consistent across all income ranges. It should also be noted that the income threshold that we used to identify low income homes failed to account for household size, which was unavailable in our data, and thus is an imperfect measure of actual household poverty. However, inasmuch as individual poverty was associated with increased CKD prevalence we suspect that more precise estimates of individual poverty would give results consistent with those we report here.
Further, although its use as a measure of neighborhood impoverishment has been extensively validated for studies like ours [31
], it should be noted that census tract poverty might not accurately reflect the neighborhood environment as experienced by our subjects. It is also possible that, as kidney disease is a chronic process, residential mobility might confound the associations between race and kidney disease within communities as persons experiencing the economic burden of chronic diseases move to less affluent neighborhoods [34
As we had only a single measure of serum creatinine we cannot exclude the possibility that some individuals were misclassified with respect to CKD. There is no reason to expect that this misclassification would occur differently for blacks and whites, and thus it should attenuate, rather than amplify, the racial disparities we observed. Also, we cannot exclude the possibility that some degree of misclassification of individual and neighborhood poverty may be possible sources of bias, but we feel that this is unlikely to significantly obscure the observation that the increased prevalence of CKD among whites compared to blacks among REGARDS subjects cannot be attributed to differences in SES. Finally, and importantly, we cannot exclude the possibility of reverse causation in the current analysis and it is possible that the association between income and CKD is due to the impact of disease on family earning potential. Finally, the relevance of lower GFR as a risk factor for progression of CKD among both older blacks and whites remains unsettled and follow-up studies to ascertain the independent role of poverty in progression to ESRD are needed.
Finally, a recent publication by Crews et al. [36
]noted that blacks sampled from a single community in Maryland had an increased prevalence of eGFR of <30 ml/min/1.73 m2
. Lower SES in this population, measured by self-reported income, was associated with an increased prevalence of CKD among blacks but not whites. This observation is consistent with the failure of individual SES to account for racial disparities in the prevalence of CKD in our analysis [36
In conclusion, family income below the poverty level is a risk factor for increased prevalence of CKD in both blacks and whites. Low income did not explain the unexpected increased CKD prevalence among whites. The factors associated with poverty that contribute to these disparities remain to be identified by prospective studies of the REGARDS and other cohort populations.