Acute Kidney Injury and Early Predictive Factors in COVID-19 Patients.

Jiaye Liu,Qingxian Cai,Qing He,Fu-Sheng Wang,Liqin Sun,Tingyan Wang,Deliang Huang,Jun Chen

doi:10.3389/fmed.2021.604242

Abstract

Objectives: Our objective was to explore the incidence and early predictive factors of acute kidney injury in coronavirus disease 2019 (COVID-19) patients.Method: We established a retrospective cohort of 408 patients who were admitted to Shenzhen Third People's Hospital in Shenzhen, China, between January 1 and March 31, 2020. Clinical outcomes and renal function were monitored until April 12, 2020, with a median follow-up duration of 21 days [interquartile range (IQR) = 14–33].Results: When first admitted to hospital (baseline), 19.36% (79/408) presented renal dysfunction [estimated glomerular filtration rate (eGFR) <90 ml/min/1.73 m2]. During follow-up, 3.9% (16/408) developed acute kidney injury (AKI). Age ≥60 years [hazard ratio (HR) = 4.78, 95% CI = 1.10–20.69], PaO2/FiO2 ratio <300 (HR = 3.48, 95% CI = 1.04–11.62), and higher creatinine (HR = 1.04, 95% CI = 1.01–1.07) at baseline independently predicted the risk of AKI. Respectively, 25.0% (102/408), 3.9% (16/408), 0.5% (2/408), 1.0% (4/408), and 0.2% (1/408) experienced G2, G3a, G3b, G4, and G5 as their most severe category during hospitalization, while 69.4% (283/408) had normal eGFRs throughout the follow-up period. When finally discharged from hospital, there were 12.5% (51/408) of patients with abnormal eGFRs.Conclusions: COVID-19 patients can be at risk of AKI and continuous eGFR decline during hospitalization, which can be early predicted by baseline factors. Some individuals still had renal dysfunction when finally discharged from hospital.

Highlights

Coronavirus disease 2019 (COVID-19) is an emerging respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
A large cohort study from China revealed that 44% of COVID-19 patients developed proteinuria or hematuria, 15.5% had an increase of blood creatinine, and 14.1% presented an increase of blood urea nitrogen; these kidney dysfunction-related events were identified as independent associated factors for mortality [14]
In the subgroup of patients who had renal dysfunction at baseline, the estimated glomerular filtration rate (eGFR) categories G2, G3a, G3b, and G4 accounted for 86.1% (68/79), 11.4% (9/79), 1.3% (1/79), and 1.3% (1/79), respectively, but no patient had renal failure (G5) at baseline

Summary

Introduction

Coronavirus disease 2019 (COVID-19) is an emerging respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Most of the published articles on COVID-19 highlighted the lungs as the main organ involved in the disease [2,3,4], and a series of studies have reported data regarding injury in the liver [5,6,7], the cardiovascular system [8, 9], and the gastrointestinal tract [10]. Another study on renal histopathological analysis of 26 autopsies of patients with COVID-19 reported that immunostaining with a SARS-CoV nucleoprotein antibody was positive in the tubule epithelium [16], which provided direct evidence of the invasion of SARSCoV-2 into the kidney tissue. Systemic hypoxia, abnormal coagulation, and possible drug or hyperventilationrelevant rhabdomyolysis could contribute to kidney injury in COVID-19 patients [17, 18]

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Methods

Results