Abstract
BackgroundAcute kidney injury (AKI) is a syndrome of reduced glomerular filtration rate and/or reduced urine flow associated with mortality in corona virus disease 2019 (COVID‐19). AKI is often associated with renal tissue damage, which may lead to chronic kidney disease. Biomarkers of tissue damage may identify patients of particular risk.MethodsIn a prospective observational study of 57 patients admitted to intensive care, AKI incidence and characteristics was evaluated according to KDIGO criteria and related to days after admission. Urinary albumin, Neutrophil Gelatinase‐Associated Lipocalin (NGAL), Kidney Injury Molecule 1 (KIM‐1) and Plasma Tissue Inhibitor of MetalloProteinase 2 (TIMP‐2) were analysed in 52 patients at admission.The majority (n = 51, 89%) of patients developed AKI, and 27 (47%) patients had predominantly oliguric AKI where oliguria was more severe than plasma Creatinine increase. Severe oliguria within first 2 days after admission was common (n = 37, 65%), whereas stage 2 and 3 AKI due to Creatinine occurred later than day 2 in 67% (12/18) of cases. Renal replacement therapy was started in 9 (16%) patients, and 30‐day mortality was 28%. Urinary biomarkers were increased in a majority of patients, but did not robustly predict KDIGO stage. Most patients had microalbuminuria, and severe albuminuria (albumin Creatinine ratio > 30 mg/mmol) was found in n = 9 (17%) patients.ConclusionsA majority of patients with COVID‐19 admitted to the ICU develop AKI. The functional deficit is often low urinary volume, and initial levels of biomarkers are generally increased without clear relation to final AKI stage.
Highlights
The pandemic corona virus disease 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARSCoV-2).[1]
The aim of this study was to investigate the incidence and characteristics of acute kidney injury (AKI) in COVID-19 patients admitted to intensive care by comparing the KDIGO criteria for Creatinine increase and urine volume over time, as well as their relation to biomarkers for kidney tissue injury, glomerular and tubular function measured at admission
The main result of this study is that 89% of critically ill COVID-19 patients admitted to intensive care developed AKI
Summary
The pandemic corona virus disease 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARSCoV-2).[1] In regions affected by SARS-CoV-2, intensive care unit (ICU) admission due to Covid-19 has been dramatic, with a high proportion of patients requiring mechanical ventilation, long lengths of stay and with substantial mortality.[2] Acute kidney injury (AKI) has been found to be an independent risk factor for death in hospitalized COVID-19 patients.[3] Early reports suggested. Neutrophil Gelatinase-Associated Lipocalin (NGAL), Kidney Injury Molecule 1 (KIM-1) and Plasma Tissue Inhibitor of MetalloProteinase 2 (TIMP-2) were analysed in 52 patients at admission. The majority (n = 51, 89%) of patients developed AKI, and 27 (47%) patients had predominantly oliguric AKI where oliguria was more severe than plasma Creatinine increase. The functional deficit is often low urinary volume, and initial levels of biomarkers are generally increased without clear relation to final AKI stage
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