Abstract
A high proportion of critically ill patients with COVID-19 develop acute kidney injury (AKI) and die. The early recognition of subclinical AKI could contribute to AKI prevention. Therefore, this study was aimed at exploring the role of the urinary biomarkers NGAL and [TIMP-2] × [IGFBP7] for the early detection of AKI in this population. This prospective, longitudinal cohort study included critically ill COVID-19 patients without AKI at study entry. Urine samples were collected on admission to critical care areas for determination of NGAL and [TIMP-2] × [IGFBP7] concentrations. The demographic information, comorbidities, clinical, and laboratory data were recorded. The study outcomes were the development of AKI and mortality during hospitalization. Of the 51 individuals that were studied, 25 developed AKI during hospitalization (49%). Of those, 12 had persistent AKI (23.5%). The risk factors for AKI were male gender (HR = 7.57, 95% CI: 1.28–44.8; p = 0.026) and [TIMP-2] × [IGFBP7] ≥ 0.2 (ng/mL)2/1000 (HR = 7.23, 95% CI: 0.99–52.4; p = 0.050). Mortality during hospitalization was significantly higher in the group with AKI than in the group without AKI (p = 0.004). Persistent AKI was a risk factor for mortality (HR = 7.42, 95% CI: 1.04–53.04; p = 0.046). AKI was frequent in critically ill COVID-19 patients. The combination of [TIMP-2] × [IGFBP7] together with clinical information, were useful for the identification of subclinical AKI in critically ill COVID-19 patients. The role of additional biomarkers and their possible combinations for detection of AKI in ritically ill COVID-19 patients remains to be explored in large clinical trials.
Highlights
The clinical spectrum resulting from infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), ranges from an asymptomatic response or the development of a mild upper respiratory tract infection to critical coronavirus disease 2019(COVID-19) [1]
During the period between May and August 2020, a total of 420 individuals were admitted to the critical areas of the Institute of Respiratory Diseases (INER)
We found that the time to acute kidney injury (AKI) was significantly shorter in individuals with [tissue inhibitor of metalloproteinases-2 (TIMP-2)] × [insulin-like growth factor binding protein 7 (IGFBP7)] ≥ 0.2 ng/mL than in those with
Summary
The clinical spectrum resulting from infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), ranges from an asymptomatic response or the development of a mild upper respiratory tract infection to critical coronavirus disease 2019(COVID-19) [1]. These patients are likely to be the ones who would benefit from the use of biomarkers and early interventions In this context, the tissue inhibitor of metalloproteinases-2 (TIMP-2) and the insulin-like growth factor binding protein 7 (IGFBP7) have been identified as possible AKI biomarkers, given that both are released following ischemic or inflammatory processes in the kidney, resulting in G1 cell cycle arrest for a short period [6–8]. The tissue inhibitor of metalloproteinases-2 (TIMP-2) and the insulin-like growth factor binding protein 7 (IGFBP7) have been identified as possible AKI biomarkers, given that both are released following ischemic or inflammatory processes in the kidney, resulting in G1 cell cycle arrest for a short period [6–8] Another biomarker of early AKI is the urinary neutrophil gelatinase-associated lipocalin (NGAL), as intrarenal concentration of this protein is abruptly up-regulated soon after ischemic or nephrotoxic kidney injury [9]
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