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Review
. 2024 Jul 6;4(1):40.
doi: 10.1186/s44158-024-00175-1.

Perfusion deficits may underlie lung and kidney injury in severe COVID-19 disease: insights from a multicenter international cohort study

Alice Nova #  1 , Bairbre McNicholas #  2   3 , Aurora Magliocca  4   5 , Matthew Laffey  6 , Vanessa Zambelli  1 , Ilaria Mariani  1 , Minahel Atif  2   3 , Matteo Giacomini  4 , Giovanni Vitale  4 , Roberto Rona  7 , Giuseppe Foti  1   7 , John Laffey #  2   3 , Emanuele Rezoagli #  8   9 ; LUNG-KIDNEY Interaction Multicenter Study Group
Collaborators, Affiliations
Review

Perfusion deficits may underlie lung and kidney injury in severe COVID-19 disease: insights from a multicenter international cohort study

Alice Nova et al. J Anesth Analg Crit Care. .

Abstract

Background: Lung perfusion defects, mainly due to endothelial and coagulation activation, are a key contributor to COVID-19 respiratory failure. COVID-19 patients may also develop acute kidney injury (AKI) because of renal perfusion deficit. We aimed to explore AKI-associated factors and the independent prediction of standardized minute ventilation (MV)-a proxy of alveolar dead space-on AKI onset and persistence in COVID-19 mechanically ventilated patients.

Methods: This is a multicenter observational cohort study. We enrolled 157 COVID-19 patients requiring mechanical ventilation and intensive care unit (ICU) admission. We collected clinical information, ventilation, and laboratory data. AKI was defined by the 2012 KDIGO guidelines and classified as transient or persistent according to serum creatinine criteria persistence within 48 h. Ordered univariate and multivariate logistic regression analyses were employed to identify variables associated with AKI onset and persistence.

Results: Among 157 COVID-19 patients on mechanical ventilation, 47% developed AKI: 10% had transient AKI, and 37% had persistent AKI. The degree of hypoxia was not associated with differences in AKI severity. Across increasing severity of AKI groups, despite similar levels of paCO2, we observed an increased MV and standardized MV, a robust proxy of alveolar dead space. After adjusting for other clinical and laboratory covariates, standardized MV remained an independent predictor of AKI development and persistence. D-dimer levels were higher in patients with persistent AKI.

Conclusions: In critically ill COVID-19 patients with respiratory failure, increased wasted ventilation is independently associated with a greater risk of persistent AKI. These hypothesis-generating findings may suggest that perfusion derangements may link the pathophysiology of both wasted ventilation and acute kidney injury in our population.

Keywords: Acute kidney injury; Dead space; Mechanical ventilation; Minute ventilation; Perfusion; Respiratory failure.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Creatinine, d-dimer, WBC, and PCT during the first ICU week, stratified in no AKI, transient AKI, and persistent AKI groups. The trend in creatinine, d-dimer, WBC, and PCT over time in patients without AKI (green circles), with transient (blue triangles), and persistent (red squares) AKI. All data represent mean ± SEM. $ refers to the effect of AKI groups on the continuous variable; $$ refers to the effect of day from ICU admission on the continuous variable; $$$ refers to the interaction between AKI groups and day from ICU admission on the continuous variable. ✚P < 0.05 for comparison between no AKI and transient AKI groups; *P < 0.05 for comparison between no-AKI and persistent AKI groups; #P < 0.05 for comparison between transient and persistent AKI groups. Definition of abbreviation. PCT, procalcitonin; WBC, white blood cells
Fig. 2
Fig. 2
PaCO2, minute ventilation, and standardized minute ventilation, during the first ICU week, stratified in no AKI, transient AKI, and persistent AKI groups. The trend in PaCO2, minute ventilation, and standardized minute ventilation over time in patients without AKI (green circles), with transient (blue triangles), and persistent (red squares) AKI. All data represent mean ± SEM. $ refers to the effect of AKI groups on the continuous variable; $$ refers to the effect of day from ICU admission on the continuous variable; $$$ refers to the interaction between AKI groups and day from ICU admission on the continuous variable. ✚P < 0.05 for comparison between no-AKI and transient AKI groups; *P < 0.05 for comparison between no-AKI and persistent AKI groups; #P < 0.05 for comparison between transient and persistent AKI groups. Definition of abbreviation. PaCO2, arterial partial pressure of carbon dioxide
Fig. 3
Fig. 3
Subjects (%) stratified in no AKI/transient AKI and persistent AKI subgroups in ordinal groups of PaCO2, minute ventilation, and standardized minute ventilation. PaCO2 (mmHg): Q1 < 38.7, Q2 ≥ 38.7 - < 45.1, Q3 ≥ 45.1 - < 56.2, Q4 ≥ 56.2; minute ventilation (L/min): Q1 < 8.7, Q2 ≥ 8.7 - < 10.3, Q3 ≥ 10.3 - < 12.0, Q4 ≥ 12.0; standardized minute ventilation (L/min): Q1 < 9.6, Q2 ≥ 9.6 - < 11.8, Q3 ≥ 11.8 - < 15.3, Q4 ≥ 15.3. All data represent the percentage of subjects in the overall population (%); P values represent Cochran-Armitage trend tests and error bars represent 95% confidence intervals
Fig. 4
Fig. 4
Subjects (%) stratified in no AKI/transient AKI and persistent AKI subgroups in ordinal groups of PaO2/FiO2 ratio. PaO2/FiO2 ratio: Q1 < 85, Q2 ≥ 85 - < 114, Q3 ≥ 114 - < 157, Q4 ≥ 157. All data represent the percentage of subjects in the overall population (%). P values represent Cochran-Armitage trend tests, and error bars represent 95% confidence intervals
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