Background To investigate the temporal characteristics of clinical variables of hospital-acquired acute kidney injury (AKI) in COVID-19 patients and to longitudinally predict AKI onset. Methods There were 308 hospital-acquired AKI and 721 non-AKI (NAKI) COVID-19 patients from Stony Brook Hospital (New York, USA) data, and 72 hospital-acquired AKI and 303 NAKI COVID-19 patients from Tongji Hospital (Wuhan, China). Demographic, comorbidities, and longitudinal (3 days before and 3 days after AKI onset) clinical variables were used to compute odds ratios for and longitudinally predict hospital-acquired AKI onset. Results COVID-19 patients with AKI were more likely to die than NAKI patients (31.5% vs 6.9%, adjusted p < 0.001, OR = 4.67 [95% CI 3.1, 7.0], Stony Brook data). AKI developed on average 3.3 days after hospitalization. Procalcitonin was elevated prior to AKI onset ( p < 0.05), peaked, and remained elevated ( p < 0.05). Alanine aminotransferase, aspartate transaminase, ferritin, and lactate dehydrogenase peaked the same time as creatinine, whereas d -dimer and brain natriuretic peptide peaked a day later. C-reactive protein, white blood cell and lymphocyte showed group differences − 2 days prior ( p < 0.05). Top predictors were creatinine, procalcitonin, white blood cells, lactate dehydrogenase, and lymphocytes. They predicted AKI onset with areas under curves (AUCs) of 0.78, 0.66, and 0.56 at 0, − 1, and − 2 days prior, respectively. When tested on the Tongji Hospital data, the AUCs were 0.80, 0.79, and 0.77, respectively. Conclusions Time-locked longitudinal data provide insight into AKI progression. Commonly clinical variables reasonably predict AKI onset a few days prior. This work may lead to earlier recognition of AKI and treatment to improve clinical outcomes.
Acute kidney injury (AKI) is associated with high mortality in coronavirus disease 2019 (COVID-19). However, it is unclear whether patients with COVID-19 with hospital-acquired AKI (HA-AKI) and community-acquired AKI (CA-AKI) differ in disease course and outcomes. This study investigated the clinical profiles of HA-AKI, CA-AKI, and no AKI in patients with COVID-19 at a large tertiary care hospital in the New York City area. The incidence of HA-AKI was 23.26%, and CA-AKI was 22.28%. Patients who developed HA-AKI were older and had more comorbidities compared to those with CA-AKI and those with no AKI (p < 0.05). A higher prevalence of coronary artery disease, heart failure, and chronic kidney disease was observed in those with HA-AKI compared to those with CA-AKI (p < 0.05). Patients with CA-AKI received more invasive and non-invasive mechanical ventilation, anticoagulants, and steroids compared to those with HA-AKI (p < 0.05), but patients with HA-AKI had significantly higher mortality compared to those with CA-AKI after adjusting for demographics and clinical comorbidities (adjusted odds ratio = 1.61, 95% confidence interval = 1.1–2.35, p < 0.014). In addition, those with HA-AKI had higher markers of inflammation and more liver injury (p < 0.05) compared to those with CA-AKI. These results suggest that HA-AKI is likely part of systemic multiorgan damage and that kidney injury contributes to worse outcomes. These findings provide insights that could lead to better management of COVID-19 patients in time-sensitive and potentially resource-constrained environments.
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