ABSTRACT
Background: Coronavirus disease-2019 (COVID-19) has the highest mortality in patients with advanced age and those with pre-existing chronic medical conditions. Limited data, however, is available with regard to COVID-19 mortality in acute kidney injury (AKI). We aimed to identify risk factors associated with mortality in patients hospitalized for COVID-19 with AKI. Methods: This is a retrospective cohort study conducted at Loma Linda University Medical Center (LLUMC) from March 1st, 2020 to January 31st, 2021. Inclusion criteria included patients admitted to LLUMC with diagnosis of COVID-19 and AKI during the admission based on the Risk Injury Failure Loss ESRD (RIFLE) criteria. Univariable and multivariable logistic regression models were utilized to explore risk factors associated with in-hospital mortality. Results: A total of 320 patients (age 66.5 ± 14.4) were included in the analysis, of which 88 (28%) were deceased. Multivariable regression analysis (Figure 1) demonstrated that age greater than 70 had adjusted odds ratio (OR) with 95% confidence interval (CI) for mortality 1.10 (95% CI: 1.01, 1.20, p=0.03). An Ejection Fraction of less than 50% had OR=1.13 (95% CI: 1.03, 1.23, p=0.01), AKI-injury stage had OR=1.25 (95% CI: 1.14, 1.37, p=<0.001), positive D-dimer levels had OR=1.18 (95% CI: 1.07, 1.30, p=<0.001) and diabetes had OR=1.12 (95% CI 1.03, 1.22, p=0.01), all significant risk factors for mortality. In addition, Hispanics had a higher risk of mortality with OR=1.20 (95% CI 1.09, 1.33, p=<0.001) when compared to Caucasians. Conclusions: Diabetes, age greater than 70, Hispanic background, Heart failure with reduced ejection fraction, AKI-injury stage, and positive D-dimer level are identified as risk factors associated with higher mortality amongst patient admitted with COVID-19 and AKI.
ABSTRACT
Introduction: The relationship between COVID-19 infection and the activation of a wide spectrum of pro-inflammatory and pro-thrombotic mechanisms such as antiphospholipid syndrome (APS) and Thrombotic Microangiopathy (TMA) is not yet well understood. However, there is emerging evidence on the link between COVID-19 and TMA. Here, we report a case of a biopsy-proven chronic TMA following COVID-19 infection. Case Description: A 48-year-old Hispanic female with a past medical history of diabetes, and hypothyroidism, who was recently discharged from the hospital following a COVID-19 infection (complicated by ICU admission requiring intubation about a month ago), presented with severe abdominal pain. No prior history of miscarriage in the past;the patient has two kids with uneventful pregnancies. Denies any family history of autoimmune disease. Initial workups indicated that splenic and renal infarcts concerning primary antiphospholipid syndrome were further supported by positive serological testing confirming the presence of positive Antineutrophil antibody, Cardiolipin antibody, B2glycoprotein, and Lupus anticoagulant. In addition, the urinalysis showed active urinary sediment with dysmorphic RBCs and nephrotic range proteinuria. The patient had a kidney biopsy which was consistent with chronic TMA and was initiated on anticoagulation therapy with warfarin for antiphospholipid antibody syndrome. Discussion: The possibility of occurrence of TMA following COVID-19 infection and the possible association between markers of endothelial activation, intravascular hemolysis, coagulation and organ damage in infection should be considered. This understanding is clinically relevant as it may necessitate the need for early APS antibody and TMA panel testing and initiation of anticoagulation in the amplified hypercoagulable state in COVID-19, especially in preventing life-threatening thrombosis.