Previous studies have reported that Black patients have a disproportionately higher risk of AKI when compared with White patients [4,8,16,17,18,19,20,21,22]. Using self-reported Black and White participants from the Atherosclerosis Risk in Communities (ARIC) study, Grams et al. [4] investigated the impact of race on the incidence of AKI-related hospitalizations. The authors in the large, prospective, community-based studies involving 10,588 African-American and Caucasian participants followed up for 13 years reported significantly higher incidence of AKI in Blacks, with a 30% higher risk in Blacks compared to Whites. After a sequential multivariable model, the risk increased to 50% following the inclusion of age and sex, suggesting that Blacks are at a greater risk of AKI despite their younger age. However, the risks were not significantly different among those participants with major mediators such as obesity, diabetes, or hypertension, which are more common in Blacks compared to Whites. The authors further showed that the relationship between race and AKI was significantly weakened with adjustment for socio-economic indicators such as access to health insurance and total annual family income.

Similarly, other studies have reported significantly higher incidence of AKI along racial lines among specialized populations, including patients with diabetes [17], trauma [20], and those undergoing procedures such as percutaneous coronary intervention [8,21] and knee surgery [19].

In contrast to the findings of Grams et al. [4] in the ARIC study, Muiru and his colleagues, in the Chronic Renal Insufficiency Cohort (CRIC) Study, a multicenter prospective study, observed that Blacks had a 22% greater hazard for AKI hospitalization than the Whites, and showed that the racial disparities in AKI were due to the differences in prehospitalization baseline clinical risk factors such as diabetes, blood pressure, and proteinuria [22]. Thus, this suggested that the increased risk of AKI among Black individuals may be mitigated through targeted screening and tighter control of blood pressure to lower proteinuria. Taken together, all these findings highlight the need for future studies to untie the “Gordian knot” between socio-economic determinants of AKI from those that might be biologic, if any.

Moreover, according to the 2018 USRDS annual data report [23], using data from the Medicare, Clinformatics^TM, (OptumInsight, Eden Prairie, MN, USA) and Veterans Affairs patient population, a higher proportion of Black patients had AKI compared to Whites or Asians. Among Medicare patients aged 66 years and older, AKI incidence rates were 34.3%, 23%, and 25.9% in Black, White, and Asian patients, respectively, and for Optum Clinformatics™ (OptumInsight, Eden Prairie, MN, USA) patients aged 22 years and older, the incidence of AKI among Black, White, and Asian patients was 9.4%, 7.4%, and 3.3%, respectively. The hospitalized Veterans Affairs populations showed a similar trend—the incidence of AKI was 30.4%, 24.1%, and 24.2% among Black, White, and Asian Americans, respectively. These data therefore highlight differences in AKI incidence by race. 

Considering the well-established genetic susceptibility for kidney disease among Black populations [33,34], it was not surprising that Privratsky et al. [35] demonstrated a greater-than-two-fold rise in postoperative serum creatinine among Black patients with high-risk APOL1 status undergoing cardiac surgery. However, a previous study by Grams et al. [4] showed that APOL1 high-risk variant was not significantly associated with higher risk of AKI. This study was limited by reliance on billing codes to ascertain AKI, thereby resulting in ill-defined AKI phenotypes. Given that there are several recent reports of association between high-risk APOL1 status and increased risk of AKI among patients infected with severe acute respiratory coronavirus 2 (SARS-CoV-2) [35,36,37,38,39,40,41], further studies are needed to elucidate APOL1 biology, its role in well-defined AKI cases, and its possible modifying effect on progression to CKD after injury.

Acute kidney injury is a well-recognized complication of SARS-CoV-2 infection, with an incidence rate of 20% among hospitalized patients and greater than 50% among the critically ill patients [42]. Since the first case of SARS-CoV-2 infection which causes coronavirus disease 2019 (COVID-19) was reported in Wuhan, China, racial disparities in the development, severity, and outcomes of this disease have become increasingly reported [43,44,45]. According to the Centers for Disease Control, Blacks had a 1.1 times higher rate of COVID-19 patients, 2.3 times higher rate of COVID-19 hospitalization, and 1.7 times higher COVID-19 mortality rate than Whites [46]. Accordingly, several previous studies have reported that Black patients with COVID-19 had approximately 1.2–2.2 times increased odds of developing in-hospital AKI compared to their White counterparts [47,48,49,50]. Even though the exact mechanism of racial disparities in risk of COVID-associated AKI is yet to be elucidated, some possible mechanisms have been proposed. Genetic polymorphisms involving ACE2, IL-6, and AChE genes are closely associated with higher burden of COVID-19 disease and these gene polymorphisms have been shown to be more common in Black individuals [51,52]. In addition, Black populations are exposed to a higher risk of vitamin D deficiency, and it has been proposed that Vitamin D plays a protective role against COVID-19 infectivity and severity through its ability to modulate the immune system by suppressing T helper-1 functions and potentiating expression of the regulatory T cells, thereby causing less severe cytokine storm [53,54]. Hence, Black patients may face higher risk of cytokine storm and associated systemic and intrarenal inflammation.