Abstract
PurposeThis study investigated the incidence, disease course, risk factors, and mortality in COVID-19 patients who developed both acute kidney injury (AKI) and acute cardiac injury (ACI), and compared to those with AKI only, ACI only, and no injury (NI).MethodsThis retrospective study consisted of hospitalized COVID-19 patients at Montefiore Health System in Bronx, New York between March 11, 2020 and January 29, 2021. Demographics, comorbidities, vitals, and laboratory tests were collected during hospitalization. Predictive models were used to predict AKI, ACI, and AKI-ACI onset. Longitudinal laboratory tests were analyzed with time-lock to discharge alive or death.ResultsOf the 5,896 hospitalized COVID-19 patients, 44, 19, 9, and 28% had NI, AKI, ACI, and AKI-ACI, respectively. Most ACI presented very early (within a day or two) during hospitalization in contrast to AKI (p < 0.05). Patients with combined AKI-ACI were significantly older, more often men and had more comorbidities, and higher levels of cardiac, kidney, liver, inflammatory, and immunological markers compared to those of the AKI, ACI, and NI groups. The adjusted hospital-mortality odds ratios were 17.1 [95% CI = 13.6–21.7, p < 0.001], 7.2 [95% CI = 5.4–9.6, p < 0.001], and 4.7 [95% CI = 3.7–6.1, p < 0.001] for AKI-ACI, ACI, and AKI, respectively, relative to NI. A predictive model of AKI-ACI onset using top predictors yielded 97% accuracy. Longitudinal laboratory data predicted mortality of AKI-ACI patients up to 5 days prior to outcome, with an area-under-the-curve, ranging from 0.68 to 0.89.ConclusionsCOVID-19 patients with AKI-ACI had markedly worse outcomes compared to those only AKI, ACI and NI. Common laboratory variables accurately predicted AKI-ACI. The ability to identify patients at risk for AKI-ACI could lead to earlier intervention and improvement in clinical outcomes.
Highlights
Acute kidney injury (AKI) and acute cardiac injury (ACI) are well-recognized complications of coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1–3]
It has been hypothesized that SARS-CoV2 may directly induce AKI and ACI as the kidney and heart have a high density of angiotensin-converting enzyme 2 (ACE2) receptors
ATLAS, a web-based tool developed by the Observational Health Data Sciences and Informatics (OHDSI) community that enables navigation of patient-level, observational data in the Common Data Model (CDM) format, was used to search vocabulary concepts and facilitate cohort building
Summary
Acute kidney injury (AKI) and acute cardiac injury (ACI) are well-recognized complications of coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1–3]. AKI and ACI separately have been associated with increased risk of critical illness and mortality in COVID-19 patients [1–3]. The mechanisms underlying the high incidence of AKI and ACI and their association with poor outcomes in COVID-19 are not wellunderstood and are likely multifactorial. It has been hypothesized that SARS-CoV2 may directly induce AKI and ACI as the kidney and heart have a high density of ACE2 receptors. Indirect effects of COVID-19 that contribute to AKI and ACI include hypoxia, hypotension, inflammation, thromboembolism, cytokine storm, and sepsis [1– 3, 6, 7]. Endothelial dysfunction has been reported in patients with severe COVID-19 [8] and likely plays a role in AKI and ACI
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