Before the conference, topics were selected and work groups assembled. Groups identified the key questions and conducted a systematic literature search. During the conference, work groups assembled in breakout sessions, as well as plenary sessions where their findings were presented, debated, and refined. Key questions were identified by the group and subgroups deliberated on these questions, bringing forth recommendations to the group as a whole. Deliberations followed 3 days of discussion among 32 attendees.
Summary statements were then developed by the entire group as reported here. The Steering Committee assembled an expert panel, which was divided into five smaller working groups: i definition and classification, ii epidemiology, iii diagnostic biomarkers, iv prevention, and v treatment. We unanimously agreed that a consensus definition was needed to highlight the coexistence of cardiac and renal disorders and to identify the time course of heart—kidney interaction and the primacy of the organ leading to the syndrome.
The goal of this definition would be to facilitate epidemiological studies, identify target populations for intervention, develop diagnostic tools, prevent and manage different syndromes. We chose a broad term, using the plural cardio-renal syndromes, CRS , to indicate the presence of multiple syndromes. We chose subtypes to recognize primary organ dysfunction cardiac vs. We added an additional subtype to capture systemic conditions affecting both organs simultaneously.
We chose definitions to include accepted criteria published by national and international societies. We considered definitions from the literature and used a specific publication 4 as template. Pathophysiology and definitions of the five subtypes of cardio-renal syndrome modified by Ronco et al. We chose the term CRS to indicate the bidirectional nature of the various syndromes and to recognize that this term was already established in the medical lexicon, despite lack of formal definition.
These patients experience higher mortality and morbidity, and increased length of hospitalization. Chronic abnormalities in heart function leading to kidney injury or dysfunction. This subtype refers to a more chronic state of kidney disease complicating chronic heart disease. This subtype refers to abnormalities in cardiac function secondary to AKI. The pathophysiological mechanisms likely go beyond simple volume overload and the recent consensus definition of AKI 12 may help to investigate this syndrome further.
This subtype refers to disease or dysfunction of the heart occurring secondary to CKD. There is a graded and independent association between the severity of CKD and adverse cardiac outcomes. Examples include sepsis, systemic lupus erythematosus, diabetes mellitus, amyloidosis, or other chronic inflammatory conditions. The ADQI working group recognized that many patients may populate or move between subtypes during the course of their disease.
The group discussed and considered further sub-classification, to include situations of transient or reversible dysfunction, slowly or acutely progressive vs. In cardio-renal syndromes, there are two important aspects: the first is the sequence of organ involvement and the second is the bi-directionality of signalling leading to a vicious cycle. Another important aspect is the time frame in which the derangements occur chronic or acute. In all cases, there are moments in which prevention is possible, in others mitigation of the insult is potentially feasible, in others, therapeutic strategies must be implemented.
At different times, a crucial role is played by imaging techniques and biomarkers enabling the clinician to make an early diagnosis, establish illness severity, and to potentially predict outcomes. This flowchart describes a series of conditions indicating that patients may move from one type to another of cardio-renal syndromes. Cardio-renal syndromes are characterized by significant heart—kidney interactions that share similarities in pathophysiology. However, they are also likely to have important discriminating features, in terms of predisposing or precipitating events, natural history, and outcomes.
A description of the epidemiology of heart—kidney interaction, stratified by the CRS subtypes, is a critical initial step towards understanding the overall burden of disease for each CRS subtype and vital in determining the presence of gaps in knowledge and helping design future trials. A large body of literature has examined AKI due to worsening heart function. This broad range is largely attributable to variations in the definitions of WRF, the observed time-at-risk and the population under study.
This finding was apparent across the spectrum of systemic blood pressure, pulmonary capillary wedge pressure, cardiac index, and estimated glomerular filtration rates. Chronic heart disease and CKD frequently co-exist, and often the clinical scenario does not permit to distinguish which disease came first. Large database studies do not distinguish between type 2 and type 4 CRS.
Nevertheless, between 45 and In selected circumstances, long-standing CHD results in adaptive alterations in kidney perfusion and neurohormonal activation. Kidney dysfunction was observed even among CHD patients with simple anatomical cardiac defects. A further challenge in describing the epidemiology of type 2 CRS is that patients may also transition between type 1 and type 2 CRS at various time points. Defining the epidemiology of acute reno-cardiac syndrome type 3 is challenging for several reasons: i considerable heterogeneity in predisposing conditions, ii different methods for defining AKI, iii variable baseline risk for the development of acute cardiac dysfunction i.
Cardiorenal Syndromes in Critical Care
Accordingly, incidence estimates and clinical outcomes of acute cardiac dysfunction secondary to AKI are largely context and disease-specific. Toxaemia, fluid and sodium retention, humoral mediators, and electrolyte derangements may all contribute to acute dysfunction of the heart.
This discrimination may have relevance as these two presentations may be characterized by important differences in epidemiology, risk factors, associated outcomes, and need for differing therapeutic interventions. Several observational studies have evaluated the cardiovascular event rates and outcomes in selected CKD populations. Several observational studies have found graded increases in the prevalence of CVD and heart failure HF , along with higher risk of subsequent cardiac events associated with degree of decline in kidney function. There are limited data on the epidemiology of secondary CRS type 5 due to the large number of potential contributing acute and chronic systemic conditions.
We recognize that several chronic systemic illnesses i. Importantly, in this context, there is currently an incomplete understanding of the pathophysiological mechanisms of secondary heart—kidney interactions. A prototypical condition that may lead to CRS type 5 is sepsis. The consensus group deliberated on the role of biomarkers in the diagnosis of the different types of the syndrome. The intention was to integrate biomarkers into the diagnosis of the various CRS, especially those that deal with AKI on top of acute cardiac disease. If biomarkers are to be clinically useful in these settings, physicians must be able to answer the following questions: i can biomarkers be used to early identify and classify CRS?
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Moreover, they have shown prognostic utility in patients with various stages of renal insufficiency, 75 , 76 demonstrating potential applications in CRS types 2 and 4. Although many previous studies support the usefulness of BNP in the diagnosis and management of HF patients, 77 , 78 the relationship between BNP, renal function, and the severity of HF is less clear.
Neutrophil gelatinase-associated lipocalin NGAL seems to be one of the earliest kidney markers of ischaemic or nephrotoxic injury in animal models and is detected in the blood and urine of humans soon after AKI. Cystatin C appears to be a better predictor of glomerular function than serum creatinine in patients with CKD. Kidney injury molecule-1 KIM-1 is a protein detectable in the urine after ischaemic or nephrotoxic insults to proximal tubular cells. Interleukin IL is a pro-inflammatory cytokine detected in the urine after acute ischaemic proximal tubular damage.
Of the biomarkers presented above, NGAL urine and plasma and Cystatin C are most likely to be integrated into clinical practice in the near future. Clinical trials will be needed to see if earlier identification of AKI and the use of specific treatment algorithms based on these markers will improve prognosis. There is a general agreement that bioimpedance vector analysis BIVA may contribute to a better definition of the patient's hydration status.
In this way, patients will be kept within the narrow window of adequate hydration preventing worsening of both kidney and heart function. Imaging techniques have an additional role with respect to the laboratory biomarkers in CRS. They may enhance, extend, and refine our ability to quantify renal damage and function. In patients affected by suspected CRS, it is prudent to avoid the use of iodinated contrast media if not strictly necessary.
Also in the future, non-invasive imaging techniques should be refined to quantify renal blood flow. Such data can then be correlated with cardiac and renal biomarkers and most importantly guide ongoing therapy designed to optimize renal blood flow and ultimately preserve kidney function.
Cardiorenal Syndromes: Pathophysiology to Prevention
As for type 1 CRS, venous congestion and high CVP seem to be associated with impaired renal function and independently related to all-cause mortality in a broad spectrum of patients with cardiovascular disease. The rationale for the prevention of CRS is based on the concept that once the syndrome begins it is difficult to interrupt, not completely reversible in all cases, and associated with serious adverse outcomes.
We approached prevention using a proposed classification system. These call for blood pressure control, use of drugs that block the renin—angiotensin—aldosterone system, beta-adrenergic blockers BB , coronary artery disease risk factor modification, and compliance with dietary and drug treatments. In this setting, therapies that improve the natural history of chronic HF include angiotensin converting enzyme inhibitors ACE-I , angiotensin receptor blockers ARB , BB, aldosterone receptor blockers, combination of nitrates and hydralazine, and cardiac re-synchronization therapy.
The clinical problem in many cases is sodium and water retention. Avoidance of hypervolaemia should help prevent cardiac decompensation. In addition, uremic changes, hyperkalaemia, and mediators of inflammation can have adverse cardiac consequences. Contrast-induced AKI in most cases is asymptomatic , and unlikely to cause cardiac dysfunction. Type 4 CRS is a common syndrome since it involves the progression of CKD, often due to diabetes mellitus and hypertension, with accelerated calcific atherosclerosis, progressive LVH, and the development of diastolic and systolic dysfunction.
A core concept is that treatment of the primary illness diabetes mellitus, amyloidosis, sepsis, rhabdomyolysis, haemorrhagic shock, etc.
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Both abnormal renal function and also a deterioration early in the course of treatment of ADHF increase mortality. Thus, any treatment for HF should have a neutral effect or preferably improve renal function. However, loop diuretics predispose to electrolyte imbalances, and hypovolaemia leading to neurohumoral activation, reduced renal glomerular flow with further rises in serum urea and creatinine.
Vasopressin receptor 2 antagonists can improve hyponatraemia, but without any clear survival benefit. In cardiogenic shock, treatments are designed to increase cardiac output and restore renal blood flow. Although inotropic drugs, typically dobutamine or dopamine, may tide patients over, they are often associated with increased mid-term mortality.
Depending upon pre-existing co-morbidity and the underlying aetiology, left ventricular assist devices as a bridge to transplantation or cardiac surgery may be appropriate. Self-care management is an important strategy in CHF, encompassing adherence to treatment, symptom recognition, and lifestyle changes diet and nutrition, smoking cessation, exercise training.
Angiotensin converting enzyme inhibitors, beta-blockers, ARBs, and aldosterone antagonists significantly reduce mortality and morbidity in CHF. The optimal approach is to combine ACE-I and beta-blocker, titrate dosages, to which either an ARB or aldosterone antagonist is subsequently added depending on clinical condition and patient characteristics.
In patients unable to tolerate these agents, hydralazine and nitrates may be an option. Therapy of CHF with concomitant renal impairment is still not evidence-based, as these patients are generally excluded from CHF trials. Angiotensin converting enzyme inhibitor and ARB initiation may cause deterioration in renal function, which is frequently transient and reversible.
Patients with CKD or renal artery stenosis are at a higher risk, and careful monitoring is recommended. If renal function declines, then other secondary causes such as excessive diuresis, persistent hypotension, prescription of nephrotoxic agents or underlying renovascular disease should be excluded. Hyperkalaemia occurs with these agents and dietary restriction may be required.
Anaemia is often present in patients with type 2 CRS, and correction of anaemia may improve symptoms without increasing survival. As previously discussed, type 3 CRS has only recently been recognized as a clinical entity, hence there is little known about the treatment of this complication. Since a typical clinical scenario would include AKI following contrast exposure, or following cardiovascular surgery CSA-AKI , prevention likely affords a better chance to improve outcome than treating established disease.
To prevent contrast nephropathy, many potential preventive strategies have been studied, and available evidence indicates that isotonic fluids have been the most successful intervention to date, with conflicting data surrounding N -acetylcysteine. Germane to the discussion of CRS, they identified that patients suffering AKI secondary to contrast were almost twice as likely to suffer downstream adverse events, including cardiovascular events, in the year following the contrast exposure, indicative of the serious consequences of type 3 CRS.
In terms of prevention of CSA-AKI, in a recent prospective, double-blind study of patients with left ventricular dysfunction undergoing cardiac surgery, nesiritide was associated with improved post-operative renal function compared with patients without nesiritide, thus suggesting a renoprotective property. The aim of the ADQI consensus conference on CRS was to facilitate better understanding of their epidemiology, opportunities for early diagnosis through biomarkers, development of preventive strategies, and application of evidence-based management strategies where available.
A further aim was to allow identification of gaps in the literature and provide direction for future research including clinical trials.
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We have defined five syndromes that can now be the target of future studies, described series of biomarkers which may facilitate the identification and treatment of such syndromes and have outlined general strategies for prevention and management. We hope this document will serve as starting point for focused research into the care of these conditions which affect so many people worldwide.
Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents. Oxford Academic. Google Scholar. Peter McCullough. Stefan D. Inder Anand. Nadia Aspromonte.
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Rinaldo Bellomo. Tomas Berl. Ilona Bobek. Dinna N. Luciano Daliento. Andrew Davenport. Mikko Haapio. Hans Hillege. Andrew A. Nevin Katz. Alan Maisel. Sunil Mankad.
Pierluigi Zanco. Alexandre Mebazaa. Alberto Palazzuoli. Federico Ronco. Andrew Shaw. Geoff Sheinfeld. Sachin Soni. Giorgio Vescovo. Nereo Zamperetti. Piotr Ponikowski. Article history. Revision Received:.
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Author Index. Subject Index. Cardiorenal Syndromes in Critical Care C. Epidemiology of Acute Kidney Injury.