In our large academic health system, 82.4% of Black patients who presented to the ED were hospitalized compared to 76.7% for non-Black patients. On its own, this finding may suggest that both Black and non-Black COVID-19 patients who are sick enough to seek care in the ED have a similar likelihood of being hospitalized. However, after adjustment for age, Black COVID-19 patients in the ED were 55% more likely to be hospitalized, suggesting that, without taking racial differences in age distributions into account, we may miss disparities. In fact, our exploratory stratified analyses suggested that among the youngest patients there may be a substantial disparity, with younger Black patients being more than twice as likely as similar non-Black patients to be hospitalized. The association of race with hospitalization was not attenuated by insurance status but was attenuated by adjustment for baseline comorbid conditions and renal function at presentation. While none of our models showed any significant associations with race and mortality which is consistent with other reports [1, 2], when stratified by age, Blacks in the age group (50–64) had a twofold risk of dying, and thus, this particular age group may need particular attention in the future.
The odds of AKI was higher in Black- vs. non-Black-hospitalized COVID-19 patients; however, after adjustment for age and insurance, Black patients had even higher odds of AKI, 67% and 64%, respectively, but further adjustments for comorbidities and eGFR rendered the association between race and AKI non-statistically significant. When crude models were stratified by age, the magnitude of the association of Black vs. non-Black race with AKI was higher among younger age groups, although these associations did not achieve statistical significance. While the association of race and COVID-19-related AKI have been noted previously [14, 15] and speculated to be influenced by more severe underlying comorbidities in Blacks, our study does not confirm a significant relationship between race and comorbid factors and thus suggests there are other unmeasured factors that may play a role in these observed disparities. The pathophysiology of COVID-19-induced AKI is likely multifactorial and includes aggravation of preexisting conditions, acute inflammation, cardiorenal syndrome, hemodynamic instability, and hypovolemia [14,15,16]. Studies are ongoing to elucidate potential mechanisms and include examining the role of direct viral toxicity to the kidney and of genetic predispositions, such as APOL1 risk alleles [17].
While we seek to find the independent effect of race, it is worth considering that both the direct and indirect effects of race are important in describing disparities. Rather than being confounders of race and outcomes, the covariates we examined are likely on the causal pathway and thus mediators of the association [18]. Although we did not do a formal mediation analysis of direct and indirect effects, we can examine our sequentially adjusted models for a complete picture of racial disparity. For example, for all three outcomes, the addition of age increased the magnitude of the association of race with the outcome, which suggests that much of the effect of race is through the differing age distributions of Black vs. non-Black COVID-19 patients presenting to the ED or being hospitalized. Insurance had little effect, likely related to the lack of difference in insured status we noted in our population. As others have reported, we found that comorbidities such as obesity, hypertension, diabetes, and CKD were more prevalent in Black patients; adjustment for these lessened the magnitude (and sometimes rendered null) the associations of race with outcomes. This suggests much of the effect we see after adjustment for age is due to the differing prevalence of comorbid conditions in Black vs. non-Black populations, which is likely due to sequelae of race and associated social exposures over the life course.
Although we found that hospitalized Black patients were 44% more likely to develop AKI, it is possible that the presentation eGFR reflected those with CKD and/or those with early signs of AKI upon presentation to the ED. We were not able to determine the evidence of prior CKD, by previous eGFRs, as these data were only available for 10% of the population, and thus is a limitation of our study. In addition, the use of ICD-10 billing codes for evidence of comorbidities, particularly for CKD, may have led to misclassification. For example, it is unknown whether the CKD ICD-10 codes were based on previous known renal function or if reflective of the eGFR upon presentation to the ED which may have in fact signaled the presence of AKI.
Other limitations deserve mention. It is unknown if patients presenting to the ED may have had outpatient encounters in the earlier stages of their COVID-19 illness, especially when testing was limited. And similarly, it is not known how (or if) short-term or long-term sequela may differ between race groups. There is the potential for selection bias, given that 14% of individuals had unknown race and were dropped from the analysis. There may be other confounders or mediators, such as markers of socioeconomic status beyond insurance (which did not vary in our population), that are unknown or unmeasured. In addition, our small Hispanic cohort does not allow for evaluation of disparate outcomes in this underserved population. Other limitations include that ORs overestimate risk in the setting of common outcomes and that our stratified analyses are limited in power.
While our study lacked more detailed socioeconomic factors (e.g., income, education history, frontline worker status), we did not observe that, as a representation of lack of or delayed access to healthcare, Black patients were less likely to be insured, as has been hypothesized. Conversely, 96.7% of Black patients who presented to the ED and 98.1% of Black patients who were hospitalized had healthcare insurance (compared to 93.9% and 96.2% of non-Black patients, respectively); thus, our highly insured population could be viewed as a strength in that it allows for the examination of other putative risk factors beyond the lack of insurance coverage. Furthermore, since this report includes only patients who presented to the ED (and not outpatient clinics or urgent care centers), and insurance status might drive decisions to present to the ED and possibly be admitted to the hospital, it may have represented a sicker cohort, thus explaining the higher hospitalization risks for both racial groups, compared to other reports [1, 2].
Other strengths of our study include capturing a full 3 months of data during the initial peak of the COVID-19 pandemic in Georgia. We also include racial comparisons for all patients presenting to the ED as well as those hospitalized to better characterize the more at-risk cohort. In addition, our data analyses utilized a priori incremental modeling methods to better explain associations we observed with various exposures on the clinical outcomes. To our knowledge, this has not been fully detailed in other studies.
Our report highlights that in our highly insured cohort, Blacks and non-Blacks who present to the ED have similar risks of hospitalization and, of those who are hospitalized, similar in-hospital mortality when adjusted for multiple factors. We do find a disparity in risk for AKI in the Black cohort which needs to be further explored. However, our results also suggest that examination of disparities without exploration of the individual effects of age and comorbid conditions may mask important patterns. While our stratified analyses suggested that disparities in outcomes may differ substantially by age and comorbid conditions, further exploration among these important subgroups is needed to better target interventions to reduce disparities in clinical outcomes of COVID-19.