Dataset Information

Acute Kidney Injury in Critically-Ill COVID-19 Patients.

ABSTRACT: Acute kidney injury (AKI) is common in patients with COVID-19, however, its mechanism is still controversial, particularly in ICU settings. Urinary proteinuria profile could be a non-invasive tool of interest to scrutinize the pathophysiological process underlying AKI in COVID-19 patients. We conducted a retrospective study between March 2020 and April 2020. All patients with laboratory-confirmed COVID-19 and without end-stage kidney disease requiring renal replacement therapy before ICU admission were included. Our objectives were to assess the incidence and risk factors for AKI and to describe its clinical and biological characteristics, particularly its urinary protein profile. Seventy patients were included; 87% needed mechanical ventilation and 61% needed vasopressor during their ICU stay; 64.3% of patients developed AKI and half of them needed dialysis. Total and tubular proteinuria on day 1 were higher in patients with AKI, whereas glomerular proteinuria was similar in both groups. The main risk factor for AKI was shock at admission (OR = 5.47 (1.74-17.2), p < 0.01). Mortality on day 28 was higher in AKI (23/45, 51.1%) than in no-AKI patients (1/25, 4%), p < 0.001. Risk factors for 28-days mortality were AKI with need for renal replacement therapy, non-renal SOFA score and history of congestive heart failure. AKI is common in COVID-19 patients hospitalized in ICU; it seems to be related to tubular lesions rather than glomerular injury and is related to shock at ICU admission.

SUBMITTER: Arrestier R

PROVIDER: S-EPMC8999255 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Acute Kidney Injury in Critically-Ill COVID-19 Patients.

Arrestier Romain R Gendreau Ségolène S Mokrani David D Bastard Jean-Philippe JP Fellahi Soraya S Bagate François F Masi Paul P d'Humières Thomas T Razazi Keyvan K Carteaux Guillaume G De Prost Nicolas N Audard Vincent V Mekontso-Dessap Armand A

Journal of clinical medicine 20220405 7

Purpose: Acute kidney injury (AKI) is common in patients with COVID-19, however, its mechanism is still controversial, particularly in ICU settings. Urinary proteinuria profile could be a non-invasive tool of interest to scrutinize the pathophysiological process underlying AKI in COVID-19 patients. Material and Methods: We conducted a retrospective study between March 2020 and April 2020. All patients with laboratory-confirmed COVID-19 and without end-stage kidney disease requiring renal replace ...[more]

PMID: 35407639

Similar Datasets

Project description:ImportanceSepsis-related host-response anomalies contribute to acute kidney injury (AKI) duration. Data on the host-response specific to COVID-19-associated AKI (COVID-AKI) in critically ill patients is limited.ObjectivesWe postulated that persistent COVID-AKI (> 48 hr) differs in host response from transient (< 48 hr) or no COVID-AKI.Design, setting, and participantsThis prospective biomarker study observed patients with severe acute respiratory syndrome coronavirus 2 infection, without chronic kidney disease, in three ICUs from March 2020 to July 2020. AKI was assessed by hourly urine output and daily plasma creatinine.Main outcomes and measuresLuminex and enzyme-linked immunosorbent assay were used to analyze 48 plasma protein biomarkers across six pathophysiological domains, which were tested with mixed-effects models.ResultsOf 177 included patients, 106 (59.9%) had AKI within the first 48 hours of admission, of whom 76 (71.7%) had persistent AKI and 30 (28.3%) transient AKI. Those with persistent AKI often had obesity, hypertension, and a higher Sequential Organ Failure Assessment score due to the renal component. Longitudinal analyses revealed that seven proteins were elevated in persistent AKI compared with no AKI. These were related to inflammation (triggering receptor expressed on myeloid cells 1, p < 0.001; tumor necrosis factor receptor 1, p < 0.001; procalcitonin, p = 0.001), complement activation (mannan-binding lectin serine protease-2, p = 0.001), kidney dysfunction (cystatin C, p < 0.001; neutrophil gelatinase-associated lipocalin, p < 0.001), and lung dysfunction (Clara cell secretory protein 16, p < 0.001). AKI (duration) was not associated with differences in the cytokine signaling, endothelial cell activation, or coagulation domains.Conclusions and relevanceIn contrast with sepsis-associated AKI, primarily inflammation-related biomarker levels correlated with COVID-AKI persistence. This study offers insights into COVID-AKI and may guide approaches to mitigate its persistence.

Dataset Information

Acute Kidney Injury in Critically-Ill COVID-19 Patients.

Publications

Acute Kidney Injury in Critically-Ill COVID-19 Patients.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets