Original ContributionAcute kidney injury after cardiac arrest of ventricular fibrillation and asphyxiation swine model☆,☆☆
Introduction
Patients who survive in an initial cardiac arrest (CA) have significant morbidity and mortality [1], [2], [3], [4]. Postresuscitation morbidity is often attributed to cerebral, myocardial and prolonged, complete, whole-body ischemia-reperfusion injury (IRI) [5], which is an unnatural pathophysiologic stage created by successful cardiopulmonary resuscitation (CPR). Such ischemic injury should have major effects on the kidneys.
The acute kidney injury (AKI) is a syndrome characterized by the rapid loss of the kidney's excretory function. It is common in any cohort of critically ill patients, such as the survivors of CA. Post-CA AKI is usually considered related to the post-CA syndrome (PCAS) and might affect the long-term survival. However, it does not attract as much important as the cerebral and myocardial injury do. Serum creatinine (sCr) and urine output are the standard diagnostic indexes of the RIFLE (risk, injury, failure, loss, end stage) criteria, Acute Kidney Injury Network (the AKIN criteria), and Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guidelines for AKI [6], [7]. However, both sCr and urine output have a lack of sensitivity and/or specificity; thus, new biomarkers for earlier and more accurate detection are needed [8], [9]. Neutrophil gelatinase–associated lipocalin (NGAL), cystatin C (CysC), kidney injury molecule 1 (KIM-1), and N-asetil-β-glukosaminidase (NAG), which are the clinical utility of certain novel AKI biomarkers, already evaluated in various clinical conditions and were deemed as good as or better than creatinine (Cr) in detecting AKI, particularly in the early stage [10], [11].
In this study, we hypothesized that postresuscitation AKI was common in both ventricular fibrillation (VF) CA (VFCA) and asphyxiation CA (ASCA). The purpose of this study was to confirm this hypothesis by carrying out the biomarkers on the characteristics of renal function and structures in swine models of CA.
Section snippets
Methods
This prospective laboratory study was approved by the Capital Medical University Institutional Animal Care Committee and the Beijing Chao-Yang Hospital Affiliated to the Capital Medical University Animal Care and Use Committee. All animals received treatments in compliance with the National Research Council's 1996 Guide for the Care and Use of Laboratory Animals. Anesthesia was titrated in all surgical interventions to avoid unnecessary suffering. The study was performed according to
Characteristics of animals
The animal profile (sex and weight), time of preparatory phase, and the extra doses of propofol and fentanyl administered during the preparatory phase did not differ significantly in the 2 groups (Table 1).
Rate of ROSC and survivals
All animals in both groups had CA. The duration between clamping the tube and CA in the ASCA group was between 13 and 20 minutes (16.8 ± 1.3 minutes). Return of spontaneous circulation was observed in 100% (16/16) of animals of the VFCA group and only 50% (8/16) of animals of the ASCA group (P
Discussion
The high mortality of patients who initially achieve ROSC after CA can be attributed to PCAS that involves multiple organs, and epidemiological data suggested that the mortality of PCAS was nearly 70% [5]. Because there is no doubt about the importance of heart and brain, post-CA myocardial dysfunction and brain injury as well as the systemic IRI are always paid close attention. However, the kidney is ignored, although the injured kidneys may play a key role in the systemic derangement present
Conclusions
Our findings suggest that post-CA AKI that occurs at an early stage of postresuscitation is common in both VFCA and ASCA, but ASCA has more severe kidney injury and worse prognosis. The novel AKI biomarkers in serum and urine, such as NGAL, CysC, KIM-1, and NAG, are of significant importance as early predictors of post-CA AKI.
Acknowledgments
The authors thank Yi Zhang, Qin Yin, Zhi-Jun Guo, Shuo Wang, and Qian Zhang for excellent technical assistance.
References (22)
- et al.
Out-of-hospital cardiac arrests in the older age groups in Melbourne, Australia
Resuscitation
(2011) - et al.
Out-of hospital cardiac arrests in young adults in Melbourne, Australia
Resuscitation
(2011) - et al.
Acute kidney injury
Lancet
(2012) Biomarkers of acute kidney injury
Clin Queries: Nephrol
(2012)- et al.
Long-term risk of mortality and other adverse outcomes after acute kidney injury: a systematic review and meta-analysis
Am J Kidney Dis
(2009) Pathophysiology of ischemic acute tubular necrosis
Clin Queries: Nephrol
(2012)- et al.
Acute kidney injury after cardiac arrest
Resuscitation
(2012) - et al.
Coagulopathy after successful cardiopulmonary resuscitation following cardiac arrest: implication of the protein C anticoagulant pathway
J Am Coll Cardiol
(2005) - et al.
Regional variation in out-of-hospital cardiac arrest incidence and outcome
JAMA
(2008) - et al.
In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival
Intensive Care Med
(2007)
Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, Inter American Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa), the American Heart Association Emergency Cardiovascular Care Committee, the Council on Cardiovascular Surgery and Anesthesia, the Council on Cardiopulmonary, Perioperative, and Critical Care, the Council on Clinical Cardiology, and the Stroke Council
Circulation
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Conflicts of interests: None.
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Sources of fundation: Beijing Natural Science Foundation (No. 81372025); Technology Foundation for the Tutor of Beijing Excellent Doctoral Dissertation (No. 20121002501).