Self-identified Race and COVID-19-Associated Acute Kidney Injury and Inflammation: a Retrospective Cohort Study of Hospitalized Inner-City COVID-19 Patients

Abstract

Background: Black individuals have been disproportionately affected by the coronavirus disease 2019 (COVID-19). However, it remains unclear whether there are any biological factors that predispose Black patients to COVID-19-related morbidity and mortality.

Objective: To compare in-hospital morbidity, mortality, and inflammatory marker levels between Black and White hospitalized COVID-19 patients.

Design and participants: This single-center retrospective cohort study analyzed data for Black and White patients aged ≥18 years hospitalized with a positive SARS-CoV-2 PCR test between March 1, 2020, and August 4, 2020.

Main measures: The exposure was self-identified race documented in the medical record. The primary outcome of was in-hospital death. Secondary outcomes included intensive care unit admission, hospital morbidities, and inflammatory marker levels.

Key results: A total of 1,424 Black and White patients were identified. The mean ± SD age was 56.1 ± 17.4 years, and 663 (44.5%) were female. There were 683 (48.0%) Black and 741 (52.0%) White patients. In the univariate analysis, Black patients had longer hospital stays (8.1 ± 10.2 vs. 6.7 ± 8.3 days, p = 0.011) and tended to have higher rates of in-hospital death (11.0% vs. 7.3%), myocardial infarction (6.9% vs. 4.5%), pulmonary embolism (PE; 5.0% vs. 2.3%), and acute kidney injury (AKI; 39.4% vs. 23.1%) than White patients (p <0.05). However, after adjusting for potential confounders, only PE (adjusted odds ratio [aOR] 2.07, 95% CI, 1.13-3.79) and AKI (aOR 2.16, 95% CI, 1.57-2.97) were statistically significantly associated with Black race. In comparison with White patients, Black patients had statistically significantly higher peak plasma D-dimer (standardized β = 0.10), erythrocyte sedimentation rate (standardized β = 0.13), ferritin (standardized β = 0.09), and lactate dehydrogenase (standardized β = 0.11), after adjusting for potential confounders (p<0.05).

Conclusions: Black hospitalized COVID-19 patients had increased risks of developing PE and AKI and higher inflammatory marker levels compared with White patients. This observation may be explained by differences in the prevalence and severity of underlying comorbidities and other unmeasured biologic risk factors between Black and White patients. Future research is needed to investigate the mechanism of these observed differences in outcomes of severe COVID-19 infection in Black versus White patients.

Keywords: COVID-19; SARS-CoV-2; acute kidney injury; inflammatory marker; race.

Figure 1

Adjusted association between race and outcomes of hospitalized COVID-19 patients. Abbreviations: ARDS, acute respiratory distress syndrome; ICU, intensive care unit. Variables adjusted for in multivariate analysis were shown in the Supplemental Table 2. Patients with pre-existing ESRD were excluded in the analysis of acute kidney injury. Reference: White race.

Figure 2

Inflammatory marker levels and oxygen saturation on admission in Black and White hospitalized COVID-19 patients, stratified by age, sex, presence of acute kidney injury (AKI), and pulmonary embolism (PE). Abbreviations: AKI, acute kidney injury; PE, pulmonary embolism. Data were expressed as mean ± SEM. “*” denotes statistically significant difference between Black and White patients (p <0.05).

Figure 3

Peak inflammatory marker levels in Black and White hospitalized COVID-19 patients, stratified by age, sex, presence of acute kidney injury (AKI), and pulmonary embolism (PE). Abbreviations: AKI, acute kidney injury; PE, pulmonary embolism. Data were expressed as mean ± SEM. Data included highest levels of D-dimer, C-reactive protein, erythrocyte sedimentation rate, ferritin, lactate dehydrogenase and absolute neutrophil count, and lowest level of absolute lymphocyte count. “*” denotes statistically significant difference between Black and White patients (p <0.05).