| Autor: |
Lablad Y; Laboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles, Erasme Campus, 808 Route de Lennik, 1070 Brussels, Belgium., Vanhomwegen C; Laboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles, Erasme Campus, 808 Route de Lennik, 1070 Brussels, Belgium., De Prez E; Laboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles, Erasme Campus, 808 Route de Lennik, 1070 Brussels, Belgium., Antoine MH; Laboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles, Erasme Campus, 808 Route de Lennik, 1070 Brussels, Belgium., Hasan S; Laboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles, Erasme Campus, 808 Route de Lennik, 1070 Brussels, Belgium., Baudoux T; Laboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles, Erasme Campus, 808 Route de Lennik, 1070 Brussels, Belgium.; Department of Nephrology, Dialysis and Renal Transplantation, Erasme University Hospital, Erasme Campus, 1070 Brussels, Belgium., Nortier J; Laboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles, Erasme Campus, 808 Route de Lennik, 1070 Brussels, Belgium. |
| Abstrakt: |
In patients hospitalized for severe COVID-19, the incidence of acute kidney injury (AKI) is approximately 40%. To predict and understand the implications of this complication, various blood and urine biomarkers have been proposed, including neutrophil gelatinase-associated lipocalin (NGAL), chemokine (C-C motif) ligand 14 (CCL14), cystatin C, leucine aminopeptidase (LAP), and soluble urokinase plasminogen activator (suPAR). This study, conducted between mid-January and early May 2021, aimed to assess the diagnostic and prognostic capabilities of these biomarkers in a cohort of COVID-19 patients monitored during the initial two weeks of hospitalization. Among the 116 patients included in this study, 48 developed AKI within the first three days of hospitalization (41%), with 29 requiring intensive care unit (ICU) admission, and the overall mortality rate was 18%. AKI patients exhibited a statistically significant increase in urinary LAP levels, indicating acute tubular injury as a potential mechanism underlying COVID-19-related renal damage. Conversely, urinary NGAL and CCL-14 excretion rates did not differ significantly between the AKI and non-AKI groups. Importantly, elevated plasma suPAR and cystatin C levels upon admission persisted throughout the first week of hospitalization and were associated with unfavorable outcomes, such as prolonged ICU stays and increased mortality, irrespective of AKI development. In conclusion, this study underscores the early predictive value of urinary LAP levels in identifying acute tubular injury in COVID-19-induced AKI. Moreover, elevated plasma suPAR and cystatin C levels serve as valuable prognostic markers, offering insights into the short-term morbidity and mortality risks among COVID-19 patients, regardless of AKI occurrence. These findings shed light on the complex interplay between COVID-19, renal injury, and biomarkers with diagnostic and prognostic potential. |
