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Updated: Jul 16, 2025

A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
Published on: February 2, 2021
COVID-19-associated coagulopathy and acute kidney injury in critically ill patients
Bruno Caldin da Silva1, Ricardo Luiz Cordioli1, Bento Fortunato Cardoso Dos Santos1
1Hospital Israelita Albert Einstein, São Paulo, SP, Brazil.
Insights
Critically ill COVID-19 patients with acute kidney injury (AKI) had lower levels of natural anticoagulants, specifically antithrombin and protein C. These findings suggest a potential role for endogenous anticoagulants in AKI development in this population.
Area of Science:
- Critical care medicine
- Nephrology
- Hematology
Background:
- Thrombotic events and acute kidney injury (AKI) are prevalent complications in critically ill COVID-19 patients.
- Understanding the underlying mechanisms, particularly coagulation abnormalities, is crucial for managing these patients.
Purpose of the Study:
- To compare coagulation profiles in critically ill COVID-19 patients who developed AKI versus those who did not.
- To investigate the role of endogenous anticoagulants in the development of AKI in this patient cohort.
Main Methods:
- Coagulation tests, platelet function, fibrinolysis, and rotational thromboelastometry were performed on days 0, 1, 3, 7, and 14 post-ICU admission.
- Patients were stratified into two groups: those who developed AKI and those who did not.
Main Results:
- Patients with AKI were older and had lower baseline glomerular filtration rates.
- While D-dimer, fibrinogen, and rotational thromboelastometry results were similar between groups, antithrombin activity and protein C levels were significantly lower in patients who developed AKI.
- Lower protein C levels were observed consistently throughout the intensive care unit stay in the AKI group.
Conclusions:
- Critically ill COVID-19 patients who developed AKI demonstrated reduced levels of endogenous anticoagulants.
- Further research is warranted to elucidate the specific role of natural anticoagulants in the pathophysiology of AKI in critically ill COVID-19 patients.
Objective:
The incidence of thrombotic events and acute kidney injury is high in critically ill patients with COVID-19. We aimed to evaluate and compare the coagulation profiles of patients with COVID-19 developing acute kidney injury versus those who did not, during their intensive care unit stay.
Methods:
Conventional coagulation and platelet function tests, fibrinolysis, endogenous inhibitors of coagulation tests, and rotational thromboelastometry were conducted on days 0, 1, 3, 7, and 14 following intensive care unit admission.
Results:
Out of 30 patients included, 13 (43.4%) met the criteria for acute kidney injury. Comparing both groups, patients with acute kidney injury were older: 73 (60-84) versus 54 (47-64) years, p=0.027, and had a lower baseline glomerular filtration rate: 70 (51-81) versus 93 (83-106) mL/min/1.73m2, p=0.004. On day 1, D-dimer and fibrinogen levels were elevated but similar between groups: 1780 (1319-5517) versus 1794 (726-2324) ng/mL, p=0.145 and 608 (550-700) versus 642 (469-722) g/dL, p=0.95, respectively. Rotational thromboelastometry data were also similar between groups. However, antithrombin activity and protein C levels were lower in patients who developed acute kidney injury: 82 (75-92) versus 98 (90-116), p=0.028 and 70 (52-82) versus 88 (78-101) µ/mL, p=0.038, respectively. Mean protein C levels were lower in the group with acute kidney injury across multiple time points during their stay in the intensive care unit.
Conclusion:
Critically ill patients experiencing acute kidney injury exhibited lower endogenous anticoagulant levels. Further studies are needed to understand the role of natural anticoagulants in the pathophysiology of acute kidney injury within this population.
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