Critical Illness and Systemic Inflammation Are Key Risk Factors of Severe Acute Kidney Injury in Patients With COVID-19.
COVID-19
COVID-associated AKI
acute kidney injury
kidney failure
Journal
Kidney international reports
ISSN: 2468-0249
Titre abrégé: Kidney Int Rep
Pays: United States
ID NLM: 101684752
Informations de publication
Date de publication:
Apr 2021
Apr 2021
Historique:
received:
06
11
2020
revised:
12
12
2020
accepted:
11
01
2021
pubmed:
6
4
2021
medline:
6
4
2021
entrez:
5
4
2021
Statut:
ppublish
Résumé
Acute kidney injury (AKI) is an important complication in COVID-19, but its precise etiology has not fully been elucidated. Insights into AKI mechanisms may be provided by analyzing the temporal associations of clinical parameters reflecting disease processes and AKI development. We performed an observational cohort study of 223 consecutive COVID-19 patients treated at 3 sites of a tertiary care referral center to describe the evolvement of severe AKI (Kidney Disease: Improving Global Outcomes stage 3) and identify conditions promoting its development. Descriptive statistics and explanatory multivariable Cox regression modeling with clinical parameters as time-varying covariates were used to identify risk factors of severe AKI. Severe AKI developed in 70 of 223 patients (31%) with COVID-19, of which 95.7% required kidney replacement therapy. Patients with severe AKI were older, predominantly male, had more comorbidities, and displayed excess mortality. Severe AKI occurred exclusively in intensive care unit patients, and 97.3% of the patients developing severe AKI had respiratory failure. Mechanical ventilation, vasopressor therapy, and inflammatory markers (serum procalcitonin levels and leucocyte count) were independent time-varying risk factors of severe AKI. Increasing inflammatory markers displayed a close temporal association with the development of severe AKI. Sensitivity analysis on risk factors of AKI stage 2 and 3 combined confirmed these findings. Severe AKI in COVID-19 was tightly coupled with critical illness and systemic inflammation and was not observed in milder disease courses. These findings suggest that traditional systemic AKI mechanisms rather than kidney-specific processes contribute to severe AKI in COVID-19.
Identifiants
pubmed: 33817450
doi: 10.1016/j.ekir.2021.01.011
pii: S2468-0249(21)00012-7
pmc: PMC8007085
doi:
Types de publication
Journal Article
Langues
eng
Pagination
905-915Informations de copyright
© 2021 International Society of Nephrology. Published by Elsevier Inc.
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