Acute kidney injury: Incidence, risk factors, and outcomes in severe COVID-19 patients

Abstract

Background COVID-19 is a multisystemic disorder that frequently causes acute kidney injury (AKI). However, the precise clinical and biochemical variables associated with AKI progression in patients with severe COVID-19 remain unclear. Methods We performed a retrospective study on 278 hospitalized patients who were admitted to the ward and intensive care unit (ICU) with COVID-19 between March 2020 and June 2020, at the University Hospital, São Paulo, Brazil. Patients aged ≥ 18 years with COVID-19 confirmed on RT-PCR were included. AKI was defined according to the Kidney Disease Improving Global Outcomes (KDIGO) criteria. We evaluated the incidence of AKI, several clinical variables, medicines used, and outcomes in two sub-groups: COVID-19 patients with AKI (Cov-AKI), and COVID-19 patients without AKI (non-AKI). Univariate and multivariate analyses were performed. Results First, an elevated incidence of AKI (71.2%) was identified, distributed across different stages of the KDIGO criteria. We further observed higher levels of creatinine, C-reactive protein (CRP), leukocytes, neutrophils, monocytes, and neutrophil-to-lymphocyte ratio (NLR) in the Cov-AKI group than in the non-AKI group, at hospital admission. On univariate analysis, Cov-AKI was associated with older age (>62 years), hypertension, CRP, MCV, leucocytes, neutrophils, NLR, combined hydroxychloroquine and azithromycin treatment, use of mechanical ventilation, and vasoactive drugs. Multivariate analysis showed that hypertension and the use of vasoactive drugs were independently associated with a risk of higher AKI in COVID-19 patients. Finally, we preferentially found an altered erythrocyte and leukocyte cellular profile in the Cov-AKI group compared to the non-AKI group, at hospital discharge. Conclusions In our study, the development of AKI in patients with severe COVID-19 was related to inflammatory blood markers and therapy with hydroxychloroquine/azithromycin, with vasopressor requirement and hypertension considered potential risk factors. Thus, attention to the protocol, hypertension, and some blood markers may help assist doctors with decision-making for the management of COVID-19 patients with AKI.

Mortality and evolution between community and hospital-acquired COVID-AKI

“…We identified risk factors for the development of CA-AKI, is likely to be multifactorial, with cardiovascular comorbidity and predisposing factors as important contributors [ 27 ] including comorbidities such as diabetes, hypertension, CKD and COPD, and debilitating chronic diseases that have been universally associated with a worse evolution of COVID 19. In addition, we also identified that the severity of COVID and markers linked to inflammation, which is consistent with the pathophysiological mechanisms described in its pathology, where high inflammatory activity plays a preponderant role in kidney injury [ 34 ], evident in high levels of leukocytes (> 12 109/L) and ferritin (> 500 ng/mL), similar to ferritin levels (798 ng/mL) previously described by the Northwell COVID-19 Research Consortium [ 22 ] and similar leukocytes than the Brazilian cohort [ 20 ] cohort.…”

“…high inflammatory activity plays a preponderant role in kidney injury [34], evident in high levels of leukocytes (> 12 109/L) and ferritin (> 500 ng/mL), similar to ferritin levels (798 ng/ mL) previously described by the Northwell COVID-19 Research Consortium [22] and similar leukocytes than the Brazilian cohort [20] cohort.…”

“…Even when comparing the CA-AKI and HA-AKI KDIGO stages, there were no differences in mortality between them, results that could be contrasted with previous studies. In our cohort, the mortality of patients with AKI at 28 days was 68%, higher than that reported by the STOP-COVID Investigators group, where they described that 54.9% of AKI COVID patients in the ICU died within 28 days of ICU admission [19], and more likely to the 60.1% mortality rate reported in a Sau Paulo cohort [20]. These results can be explained by the conditions, hospital infrastructure and health system of our country compared to the US and Brazil.…”

Hydroxychloroquine administration exacerbates acute kidney injury complicated by lupus nephritis

“…As mentioned above, we found that a long-term therapeutic dose of HCQ for LN may disrupt autophagy and promote senescence in PTECs to increase the susceptibility to AKI. Recently, HCQ or CQ use in COVID-19 patients was also emphasized that these drugs may worsen AKI by inhibiting autophagy [ 47 – 49 ]. A previous study by Tang et al [ 50 ] found that short-term HCQ therapy attenuated I/R-induced AKI, although the autophagy pathway was also inhibited.…”

COVID-19: Impact in endothelial function and therapy with Mesenchymal Stromal Cells

“…Due to the high tropism of virus at tissues as heart, kidney and blood vessels has been observed in the pathophysiology of COVID-19: acute heart failure, dysrhythmia, myocarditis, thromboembolism events (arterial and venal) [7]; acute renal failure [12,13]; neurological damage such as impaired consciousness, stroke; liver dysfunction; blood dysfunction (i.e. metabolic acidosis) [6]; thrombosis [14]; septic shock and multiple organ failure [15,16].…”