Cardiac and Vascular Surgery-Associated Acute Kidney Injury: The 20th International Consensus Conference of the ADQI (Acute Disease Quality Initiative) Group.

Abstract

HomeJournal of the American Heart AssociationVol. 7, No. 11Cardiac and Vascular Surgery–Associated Acute Kidney Injury: The 20th International Consensus Conference of the ADQI (Acute Disease Quality Initiative) Group Open AccessarticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialOpen AccessarticlePDF/EPUBCardiac and Vascular Surgery–Associated Acute Kidney Injury: The 20th International Consensus Conference of the ADQI (Acute Disease Quality Initiative) Group Mitra K. Nadim, MD, Lui G. Forni, BSc, PhD, MBBS, MRCPI, AFICM, Azra Bihorac, MD, MS, Charles Hobson, MD, MHA, Jay L. Koyner, MD, Andrew Shaw, MB, George J. Arnaoutakis, MD, Xiaoqiang Ding, MD, Daniel T. Engelman, MD, Hrvoje Gasparovic, MD, PhD, FETCS, Vladimir Gasparovic, MD, Charles A. Herzog, MD, FAHA, Kianoush Kashani, MD, MSc, Nevin Katz, MD, Kathleen D. Liu, MD, PhD, MAS, Ravindra L. Mehta, MD, Marlies Ostermann, MD, Neesh Pannu, MD, Peter Pickkers, MD, PhD, Susanna Price, MB, PhD, FFICM, Zaccaria Ricci, MD, Jeffrey B. Rich, MD, Lokeswara R. Sajja, MD, MS, MCh, Fred A. Weaver, MD, MMM, Alexander Zarbock, MD, Claudio Ronco, MD and John A. Kellum, MD, MCCM Mitra K. NadimMitra K. Nadim Division of Nephrology & Hypertension, Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA Search for more papers by this author , Lui G. ForniLui G. Forni Department of Clinical & Experimental Medicine, University of Surrey, Guildford, United Kingdom Royal Surrey County Hospital NHS Foundation Trust, Guildford, United Kingdom Search for more papers by this author , Azra BihoracAzra Bihorac Division of Nephrology, Hypertension & Renal Transplantation, Department of Medicine, University of Florida, Gainesville, FL Search for more papers by this author , Charles HobsonCharles Hobson Division of Surgical Critical Care, Department of Surgery, Malcom Randall VA Medical Center, Gainesville, FL Search for more papers by this author , Jay L. KoynerJay L. Koyner Section of Nephrology, Department of Medicine, University of Chicago, IL Search for more papers by this author , Andrew ShawAndrew Shaw Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN Search for more papers by this author , George J. ArnaoutakisGeorge J. Arnaoutakis Division of Thoracic & Cardiovascular Surgery, Department of Surgery, University of Florida College of Medicine, Gainesville, FL Search for more papers by this author , Xiaoqiang DingXiaoqiang Ding Department of Nephrology, Shanghai Institute for Kidney Disease and Dialysis, Shanghai Medical Center for Kidney Disease, Zhongshan Hospital, Fudan University, Shanghai, China Search for more papers by this author , Daniel T. EngelmanDaniel T. Engelman Division of Cardiac Surgery, Department of Surgery, Baystate Medical Center, University of Massachusetts Medical School, Springfield, MA Search for more papers by this author , Hrvoje GasparovicHrvoje Gasparovic Department of Cardiac Surgery, University Hospital Rebro, Zagreb, Croatia Search for more papers by this author , Vladimir GasparovicVladimir Gasparovic Department of Medicine, University of Zagreb, Croatia Search for more papers by this author , Charles A. HerzogCharles A. Herzog Division of Cardiology, Department of Medicine, Hennepin County Medical Center, University of Minnesota, Minneapolis, MN Search for more papers by this author , Kianoush KashaniKianoush Kashani Division of Nephrology & Hypertension, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Mayo Clinic, Rochester, MN Search for more papers by this author , Nevin KatzNevin Katz Division of Cardiac Surgery, Department of Surgery, Johns Hopkins University, Baltimore, MD Search for more papers by this author , Kathleen D. LiuKathleen D. Liu Divisions of Nephrology and Critical Care, Departments of Medicine and Anesthesia, University of California, San Francisco, CA Search for more papers by this author , Ravindra L. MehtaRavindra L. Mehta Department of Medicine, UCSD Medical Center, University of California, San Diego, CA Search for more papers by this author , Marlies OstermannMarlies Ostermann King's College London, Guy's & St Thomas’ Hospital, London, United Kingdom Search for more papers by this author , Neesh PannuNeesh Pannu Division of Critical Care Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada Search for more papers by this author , Peter PickkersPeter Pickkers Department Intensive Care Medicine, Radboud University Medical Center, Nijmegen, The Netherlands Search for more papers by this author , Susanna PriceSusanna Price Adult Intensive Care Unit, Imperial College, Royal Brompton Hospital, London, United Kingdom Search for more papers by this author , Zaccaria RicciZaccaria Ricci Department of Pediatric Cardiac Surgery, Bambino Gesù Children's Hospital, Roma, Italy Search for more papers by this author , Jeffrey B. RichJeffrey B. Rich Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH Search for more papers by this author , Lokeswara R. SajjaLokeswara R. Sajja Division of Cardiothoracic Surgery, STAR Hospitals, Hyderabad, India Search for more papers by this author , Fred A. WeaverFred A. Weaver Division of Vascular Surgery, Department of Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA Search for more papers by this author , Alexander ZarbockAlexander Zarbock Department of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, Münster, Germany Search for more papers by this author , Claudio RoncoClaudio Ronco Department of Nephrology, Dialysis and Transplantation, San Bortolo Hospital, International Renal Research Institute of Vicenza, Italy Search for more papers by this author and John A. KellumJohn A. Kellum Department of Critical Care Medicine, School of Medicine, University of Pittsburgh, PA Search for more papers by this author Originally published1 Jun 2018https://doi.org/10.1161/JAHA.118.008834Journal of the American Heart Association. 2018;7:e008834IntroductionAcute kidney injury (AKI) occurs in 7% to 18% of hospitalized patients and complicates the course of 50% to 60% of those admitted to the intensive care unit, carrying both significant mortality and morbidity.1 Even though many cases of AKI are reversible within days to weeks of occurrence, data from multiple large observational and epidemiological studies over the past decade suggest a strong association between AKI and subsequent chronic kidney disease (CKD) and end‐stage renal disease (ESRD).2, 3 Patients with AKI who receive renal replacement therapy (RRT) are >3 times more likely to develop ESRD than those who do not. This rise in the number of patients who receive treatment for ESRD is a global phenomenon associated with considerable patient costs, effects on quality of life, and economic impact on society as a whole. In developing countries, most people with kidney failure have insufficient access to dialysis and/or kidney transplantation. Consequently, the development of effective approaches to the prevention, early recognition, and management of AKI is necessary to reduce the burden of CKD and ESRD.4Millions of patients undergo cardiac and vascular surgery (CVS) every year in developed countries alone. AKI is a common perioperative complication for patients undergoing both cardiac surgery5, 6, 7, 8, 9 and vascular surgery,9, 10, 11 occurring in 20% to 70% of cases depending on the type of surgery and the definition of AKI used. In addition, more and more of these patients who receive complex CVS are elderly with multiple comorbidities, which predispose to the development of AKI and potentially hasten progression to ESRD. Mortality rates among cardiovascular patients undergoing RRT are between 40% and 70%, and mortality is associated with both the severity of the initial insult and the number of episodes of AKI occurring during the hospital admission.12, 13In recent years, there have been considerable advances in our understanding of CVS‐associated AKI (CVS‐AKI). Nevertheless, despite the high prevalence, there is little consensus about how best to prevent or treat CVS‐AKI. The aim of this consensus process was to review the current literature on CVS‐AKI; to create the basis for its definition; to develop an initial understanding of its pathophysiology; to explore the potential use of biomarkers for its diagnosis; to critique current literature in the fields of prevention and treatment, so as to make recommendations for clinical practice; and to propose a framework for future research.MethodsADQI (Acute Disease Quality Initiative) is an ongoing process that produces evidence‐based recommendations on the diagnosis, prevention, and management of AKI and on various issues concerning acute dialysis and fluid management (http://www.adqi.org). The conference chairs of the 20th ADQI consensus committee (M.K.N., J.A.K., V.G., C.R., and L.G.F.) convened a panel of experts representing the relevant disciplines—cardiac surgery, vascular surgery, cardiology, nephrology, anesthesiology, and critical care—from North America, Europe, and Asia to discuss the issues related to CVS‐AKI (Data S1). The conference took place June 16 to 19, 2017, and the format of the meeting was a 2.5‐day modified Delphi method to achieve consensus, as described previously (Data S1).14Results and DiscussionPathophysiologyThe pathophysiology of CVS‐AKI is complex and poorly understood. Although patients undergoing cardiac and major vascular surgery may experience similar insults to the kidneys, many distinctions exist between these populations. Notable differences are the relative influence of cardiac dysfunction (greater in cardiac surgery) versus warm ischemia–reperfusion injury to the kidneys and increased abdominal pressures (both greater with vascular surgery). Finally, the effect of the cardiopulmonary bypass (CPB) circuit itself in the case of cardiac surgery is notable. Although animal models15, 16 of CPB and cardiac surgery–associated AKI (CS‐AKI) exist, they have not been widely applied to the study of AKI. Furthermore, although clinical studies have been conducted for >40 years, numerous knowledge gaps remain. Observational studies, animal and cell culture work, and mathematical simulations17 are currently available to predict the events likely to occur during cardiac surgery. Hemodynamic disturbances at each level of arterial blood supply dominate the discussion, and inflammatory, immunological, neurohumoral, and mechanical factors are also of significance (Figure 1).Download PowerPointFigure 1. Major pathophysiological mechanisms for the development of cardiac and vascular surgery–associated acute kidney injury (CVS‐AKI). Many common factors contribute to the development of CVS‐AKI. Hemodynamic perturbations such as exposure to cardiopulmonary bypass (CPB), cross‐clamping of the aorta, high doses of exogenous vasopressors, and blood‐product transfusion all increase the risk of AKI. Similarly, the mechanical factors outlined may be associated with renal perfusion injury following episodes of ischemia, resulting in increased oxidative stress and associated inflammation as well as embolic disease including cholesterol emboli, all of which increase the pathological burden on the kidney. Other mechanisms such as neurohormonal activation are relevant, as is the generation of free hemoglobin and the liberation of free iron perioperatively, all potentiating AKI. Associated tissue damage is reflected in a systemic inflammatory response, and all these factors contribute to a significant inflammatory response. Immune activation, the generation of reactive oxygen species, and upregulation of proinflammatory transcription factors all play roles.Hemodynamic perturbations.Perturbations in the renal blood flow may lead to an imbalance of oxygen supply and demand.18, 19 The inner stripe of the outer medullary portion of the kidney may be susceptible to ischemic damage caused by low resting po2 (10–20 mm Hg).18 During CPB, cardiac output is preserved, but the target blood pressure under such nonpulsatile conditions is unknown, and inadequate renal perfusion may contribute to AKI. However, using a mathematical model,17 the rewarming phase of CPB appeared to represent the period when the renal medulla may be at most risk because of the combination of high oxygen demand and low oxygen supply occurring at this time. Low cardiac output states during and after cardiac surgery are likely to contribute to the ischemic process, although whether low flow, low blood pressure, or oxygen delivery is the main culprit remains elusive.20 Studies of noncardiac surgery patients suggest that maintenance of sufficient mean arterial pressure is the most important hemodynamic parameter to preserve in the perioperative period21, 22; however, these patients are rarely exposed to hypothermia and hemodilution, so it remains unclear whether this finding also applies to cardiac surgery patients.The period after CPB may be relevant for the development of reperfusion injury,23 and the precise underlying mechanisms need to be fully understood so that preventive and salvage treatments may be developed to mitigate this process. Remote ischemic preconditioning (RIPC) appeared to show great promise in a study of high‐risk patients24 but has been shown to be ineffective (at least with respect to the effect sizes examined) in lower risk patients.25, 26, 27 Some controversy exists regarding the effects of propofol, which has been hypothesized to attenuate the response to RIPC.26The role of venous congestion in the development of AKI is a potential area of pathophysiological significance.28, 29 The role of high central venous pressure in congestive heart failure is well appreciated.30 The incidence of AKI in this population has led investigators to study it in the context of heart surgery, for which the problem is typically in the right heart, and vascular surgery, for which the problem may be increased abdominal compartment pressures. However, the mechanisms involved are unclear, and although “back pressure” on the glomerular apparatus has been postulated, it is unlikely that this process is the sole cause of this observation. It may be that the renal pelvis is able to compensate for a certain amount of increased venous volume before the pressure–flow relationship inside the poorly compliant renal capsule changes, in keeping with the Monro–Kellie doctrine observed in the brain.31 Whether this truly applies to the kidney is currently a matter of speculation but one that merits further study.Inflammation and immunity.The systemic inflammatory response is often observed following major surgery, with considerable variability observed between individuals, although it is recognized that a more severe response is associated with an increased risk of adverse outcomes including AKI.32, 33, 34 Unsurprisingly, CVS is often associated with such a response and may activate the inflammatory cascade through several pathways.35, 36 CVS exposes the patient to a risk profile somewhat different from most other major surgeries. CPB, cross‐clamping of the aorta, high doses of exogenous vasopressors, and high rates of exogenous blood product transfusion, for example, all enhance the risks of AKI, especially when coupled with the risk profile for AKI for most of these patients. Such exposures are associated with perturbations in renal perfusion that induce reperfusion injury following episodes of ischemia, resulting in increased oxidative stress and associated inflammation.37, 38 This process is exacerbated by the significant shunting within the kidney that results in the renal medulla and corticomedullary junction being relatively hypoxic relative to other tissues.18 In cardiac surgery, the entire cardiac output is exposed to an extracorporeal circuit, and this provides a further inflammatory insult through contact activation from the exposure of blood to the CPB circuit; although in the modern CPB circuit biocompatibility has been optimized, measures of immune activation (cytokine and chemokine levels) increase significantly after CPB.36 The generation of reactive oxygen species induces inflammation by upregulation of proinflammatory transcription factors, including NFκ‐B (nuclear factor κ‐B).39, 40 Cytokines and chemokines recruit neutrophils, macrophages, and lymphocytes into the renal parenchyma. Parenchymal infiltration and activation of these immune cells promote AKI and lead to fibrosis. Avoidance of the CPB machine in an attempt to reduce distant organ function has been successful,41 although recently published data suggest that 5‐year survival is lower with off‐pump techniques42; this may be a reflection of improved revascularization of the heart with the on‐pump technique. In the presence of concurrent sepsis, such as with bacterial endocarditis, sepsis and surgery appear to be synergistic in terms of affecting an immune response.43Iron metabolism and free hemoglobin.CVS leads to free hemoglobin liberation with the release of free iron, and this phenomenon has generated much interest regarding CS‐AKI.44, 45, 46, 47 A degree of hemolysis is inevitable whenever red blood cells come into contact with an artificial surface or with air (eg, blood scavenging systems), and this may be coupled with a prolonged period of hypothermia (sometimes as low as 18°C), which creates the perfect environment for hemolysis and liberation of free iron, leading to vasoconstriction through scavenging of nitric oxide by free hemoglobin. Indeed, evidence from a case–control study of patients who developed AKI postoperatively compared with matched controls demonstrated that plasma‐free hemoglobin was less than half that observed in the control group, providing further evidence that hemolysis and free iron may contribute to AKI development.44 Moreover, free hemoglobin and, particularly, free ferrous iron increase production of reactive oxygen species via the Fenton and Haber Weis reactions, especially as free hemoglobin and iron are sequestered within the kidney.48 Plasma‐free hemoglobin also induces HO‐1 (heme oxygenase 1) expression. HO‐1 degrades heme but increases in experimental models of AKI. Plasma HO‐1 is increased in patients who develop AKI, and CPB duration, hemolysis, and inflammation are associated with increased HO‐1 concentrations following cardiac surgery.45Other mechanisms.Oxygen free radical generation and metabolism is an area of active investigation49, 50 (and genetic predisposition to injury is important51, 52), but it is not clear whether this results in increased susceptibility to AKI or to innate impairment of the ability to repair and regenerate healthy renal tissue. The precise nature of the genetic (and epigenetic) variables involved also remains unclear. Furthermore, embolic disease is important for CS‐AKI. Cholesterol emboli53 are at risk for distal migration when a cross‐clamp is applied or released from the aorta, especially in patients with significant atherosclerosis. Moreover, intra‐aortic balloon counterpulsation devices increase the embolic load, and the fact that these devices are typically deployed in patients with severely compromised hemodynamic conditions makes it difficult to discern whether such devices are of overall benefit (by improving cardiac output) or harm (by increasing generation of emboli) to the kidney. In addition, tissue injury releases mitochondrial damage–associated molecular patterns including mitochondrial DNA, which can act as a direct activator of neutrophils, which in turn elicit a systemic inflammatory response syndrome while suppressing polymorphonuclear function. Such molecular patterns have also been seen during CPB and, as such, may participate in the pathogenesis of CVS‐AKI.54Diagnosis and Risk AssessmentPerioperative stratification for AKI.Recommendation:We recommend routine implementation of validated clinical risk‐prediction models in the preoperative assessment of all patients undergoing CVS, using estimated glomerular filtration rate (eGFR), cystatin C, and/or albuminuria to improve risk stratification of those at intermediate and high risk of AKI postoperatively (not graded).Rationale: Risk assessment is a dynamic process in which patients with fixed preoperative risk derived from underlying comorbidities are evaluated on the basis of additional and potentially modifiable risks from their clinical status before surgery. The use of currently available risk‐prediction instruments must be guided by the goals of risk assessment in each instance. Preoperative risk assessment may be useful for communicating risks associated with surgery to the patient and in implementing preventive strategies in the intra‐ and postoperative periods, for example, goal‐directed hemodynamic management, individualized blood pressure management,21 and avoidance of the use of NSAIDs for pain management. Postoperative risk assessment is geared toward early identification of AKI that may allow earlier implementation of preventive strategies. Peri‐ and postoperative risk assessment is geared toward early identification of AKI that may allow proactive treatment. An important conceptual point is that kidney injury in the setting of CVS occurs along a continuum and may relate to patient, preoperative, and intraoperative factors and the trajectory of AKI occurrence from baseline conditions; its development over a patient's clinical course should take this aspect into account (Figure 2).Download PowerPointFigure 2. Risk assessment for acute kidney injury (AKI) following cardiac and vascular surgery (CVS). This figure provides a framework for the time course of risk assessment for AKI following CVS. Risk assessment should be a continual process that is repeatedly performed in the pre‐, peri‐, and early postoperative time course, and it should incorporate clinical factors and biomarkers if available. Patients deemed to be at high risk of AKI may benefit from the implementation of kidney‐focused care to improve patient outcomes. CHF indicates congestive heart failure; COPD, chronic obstructive pulmonary disease; CPB, cardiopulmonary bypass; EF, ejection fraction; IABP, intra‐aortic balloon pump; IGFBP7, insulin‐like growth factor binding protein 7; KDIGO, Kidney Disease Initiative Global Outcome; NGAL, neutrophil gelatinase–associated lipocalin; PVD, peripheral vascular disease; TIMP2, tissue inhibitor of metalloproteinases 2. Although many risk‐prediction scores for AKI after cardiac surgery have been published, only 8 have been externally validated with C statistics ranging from 0.72 to 0.89 (Table S1).55, 56, 57, 58, 59, 60, 61 In general, these scoring systems have good discrimination in assessing low‐risk groups but relatively poor discrimination in moderate to high‐risk patients.62 There are no externally validated risk‐assessment tools specifically for AKI following vascular surgery; although Kheterpal and colleagues developed and externally validated an AKI risk score for general surgery cases that included but was not limited to vascular surgery.63, 64 The most robust cardiac surgery prediction tools with the best discrimination have used AKI requiring RRT as an outcome. This is problematic because AKI requiring dialysis, although catastrophic in this context, is relatively uncommon, occurring in 1% to 2% of all patients undergoing surgery in most programs. In addition, the decision to initiate RRT varies among clinicians. Less severe forms of AKI are commonly seen after cardiac surgery with reported rates of Kidney Disease Improving Global Outcomes (KDIGO) stage 1 AKI reported between 20% and 70% depending on the patient risk factors and the inclusion of KDIGO serum creatinine (sCr) and/or urine output (UO) criteria for AKI.7, 8, 65, 66, 67, 68 Three of the prediction rules have assessed risk of less severe forms of AKI defined using sCr criteria only.56, 58, 69 Of these, one used the RIFLE criteria of AKI,56 and another used the Acute Kidney Injury Network criteria.69The risk factors commonly identified in externally validated risk‐prediction models are shown in Figure 2. Preexisting CKD, although variably defined, is the strongest risk factor for AKI in this setting. With 2 exceptions,59, 70 most other prediction tools have used sCr to assess kidney function, which may significantly overestimate kidney function, particularly in malnourished elderly populations. The eGFR, which accounts for age, race, and sex and is subject to similar limitations, is likely a more accurate estimation of kidney function in stable, elective patients. The use of both eGFR and sCr in this context assumes steady‐state kidney function, which is frequently not the case. Newly identified risk factors such as preoperative hemoglobin (anemia/transfusion load) and proteinuria have only been incorporated in recent models, whereas other risk factors have not been rigorously studied for their incremental value when added to existing risk‐prediction models (eg, days from cardiac catheterization to surgery). All risk‐prediction tools have shown only moderate calibration, suggesting significant heterogeneity in the underlying populations.62 Because most risk‐prediction tools have been derived from clinical and administrative databases, they fail to capture acuity of illness, which may account for the calibration discrepancies and the difficulty in discrimination among the moderate‐ to high‐risk groups. Some measure or surrogate for hemodynamic stability is present in all published models whether it is characterized by surgical urgency or the presence of cardiogenic shock. It is likely that risk discrimination would improve if additional objectively defined clinical variables were included.At a minimum, all patients undergoing cardiac and vascular surgical procedures should undergo routine clinical assessment of AKI risk. This involves systematic evaluation of known susceptibilities for development of AKI such as CKD and albuminuria using preoperative sCr and urinalysis in all patients before surgery.71, 72, 73 These results will help frame individualized risk for AKI while perhaps providing insight into patients’ baseline renal function. Whenever possible, efforts should be made to obtain the patient's prior kidney‐function tests to ascertain true baseline function. In summary, the currently available preoperative risk‐assessment tools are beneficial in that they use commonly available data and identify low‐risk patients in the setting of traditional CVS. Nevertheless, they have several limitations: They are predominantly used to predict RRT.Sensitivity and specificity break down at the extremes of the spectrum.They do not account for preoperative eGFR (primarily rely on sCr alone).Intra‐ and postoperative factors play equally important roles in determining the course and severity of AKI; as such, continued risk assessment throughout the peri‐ and postoperative periods is crucial for patients at risk of AKI.Definition and diagnosis of AKI.Recommendations:We recommend that AKI should be defined by the KDIGO criteria, including both sCr and UO criteria (not graded).We recommend checking sCr immediately before surgery in all patients and utilizing sCr‐based eGFR to assess renal function in patients with steady state preoperatively so as to ascertain AKI postoperatively (not graded).We recommend repeated clinical reassessment of AKI risk within the first 12 postoperative hours incorporating intra‐ and postoperative variables (not graded).We suggest measuring biomarkers of AKI (eg, TIMP2·IGFBP7 [combination of tissue inhibitor of metalloproteinases 2 and insulin‐like growth factor binding protein 7] or NGAL [neutrophil gelatinase–associated lipocalin]) in patients at high risk of CS‐AKI (grade 2A).Rationale: The current Society of Thoracic Surgeons (STS) database defines AKI by KDIGO sCr‐based stage 3 AKI (sCr ≥3 times baseline or initiation of RRT).74 However, smaller changes in sCr are associated with adverse outcomes following CVS.75, 76, 77, 78 Given the association of stage 1 AKI (sCr 1.5 times baseline or ≥0.3‐mg/dL increase within 48 hours) with adverse outcomes in multiple settings, it is important to recognize stage 1 AKI (based on sCr and/or UO criteria) so that the progression to stage 2 (sCr 2.0 times baseline) or stage 3 AKI and other outcomes can be monitored. In addition, sCr criteria alone may miss ≈30% of patients with AKI, resulting in both misclassification of AKI severity and delay in management. Critically ill patients who meet AKI criteria by both sCr and UO are at higher risk of adverse outcomes including 30‐day mortality and need for RRT in comparison to those who meet a single criterion for AKI.5, 79, 80, 81 The STS database does not distinguish between AKI and acute kidney disease, which is currently defined as the course of the AKI syndrome in those who continue to have renal pathophysiological changes 7 days after the inciting event. Acute kidney disease may last for weeks to months with variable outcomes (full or partial recovery, ESRD).82 Moreover, the timing and trajectory of AKI (<7 days versus 7–30 days) after CVS can provide insight into the cause of kidney dysfunction and may likely have different associations with adverse outcomes.We recommend checking sCr in all patients to determine preoperative baseline kidney function. The time frame depends on the presence of acute illness and other factors that may affect kidney health (eg, recent exposure to iodinated contrast in the setting of cardiac catheterization, m