Cardiorenal Syndromes in Critical Care

C. Ronco, R. Bellomo, P. A. McCullough

• Editore: S. Karger
• Anno: 2010
• ISBN:
  9783805594738
• Argomento: Medicine
• Categoria: Nephrology

Critical care nephrology is an emerging multidisciplinary science in which the competences of different specialists are merged to provide a unified diagnostic and therapeutic approach to the critically ill patient. The volume at hand places great emphasis on cardiorenal syndromes and the multidisciplinary collaboration between cardiology and nephrology. Several contributions describe the cardiorenal syndrome in its different varieties and subtypes and report the results from the most recent Acute Dialysis Quality Initiative Consensus Conference, as well as proposing new diagnostic approaches based on early biomarkers of AKI. Other papers discuss advances in technology for renal replacement therapy and multiple organ support therapy. Moreover, special emphasis is placed on the potential role of extracorporeal therapies in patients affected by H1N1 influenza, and a summary of the most recent trials in the field is included.Containing the proceedings of the 2010 International Vicenza Course on Critical Care Nephrology, this publication is a state-of-the-art appraisal of today's technology and current issues related to cardiorenal syndromes.

Cardiorenal Syndromes

Ronco C, Bellomo R, McCullough PA (eds): Cardiorenal Syndromes in Critical Care.
Contrib Nephrol. Basel, Karger, 2010, vol 165, pp 54–67

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Cardiorenal Syndromes: An Executive Summary from the Consensus Conference of the Acute Dialysis Quality Initiative (ADQI)

Claudio Ronco^a · Peter A. McCullough^b · Stefan D. Anker^c · Inder Anand^d · Nadia Aspromonte^e · Sean M. Bagshaw^f · Rinaldo Bellomo^g · Tomas Berl^h · Ilona Bobek^a · Dinna N. Cruz^a · Luciano Dalientoⁱ · Andrew Davenport^j · Mikko Haapio^k · Hans Hillege^l · Andrew House^m · Nevin M. Katzⁿ · Alan Maisel^o · Sunil Mankad^p · Pierluigi Zanco^q · Alexandre Mebazaa^r · Alberto Palazzuoli^s · Federico Roncoⁱ · Andrew Shaw^t · Geoff Sheinfeld^u · Sachin Soni^a,v · Giorgio Vescovo^w · Nereo Zamperetti^x · Piotr Ponikowski^y for the Acute Dialysis Quality Initiative (ADQI) consensus group^*

^aDepartment of Nephrology, Dialysis & Transplantation, International Renal Research Institute, San Bortolo Hospital, Vicenza, Italy; ^bDepartment of Medicine, Divisions of Cardiology, Nutrition and Preventive Medicine, William Beaumont Hospital, Royal Oak, Mich., USA; ^cDivision of Applied Cachexia Research, Department of Cardiology, Charité-Universitätsmedizin, Berlin, Germany; ^dDepartment of Cardiology, VA Medical Center, Minneapolis, Minn., USA; ^eDepartment of Cardiology, St Spirito Hospital, Rome, Italy; ^fDivision of Critical Care Medicine, University of Alberta Hospital, Edmonton, Alta., Canada; ^gDepartment of Intensive Care, Austin Hospital, Melbourne, Australia; ^hDepartment of Nephrology, University of Colorado Health Sciences Center, Denver, Colo., USA; ⁱDepartment of Cardiology, University of Padua, Padua, Italy; ^jUCL Center for Nephrology, Royal Free & University College Medical School, London, UK; ^kDivision of Nephrology, Helsinki University Central Hospital, Helsinki, Finland; ^lTrial Coordination Center, Department of Cardiology and Epidemiology, University Medical Center Groningen, Hanzeplein, Netherlands; ^mDivision of Nephrology, London Health Sciences Centre, University Hospital, London, Ont., Canada; ⁿDepartment of Surgery, George Washington University, Washington, DC, USA; ^oDepartment of Medicine and Cardiology, San Diego VA Medical Center and University of California, San Diego, Calif., USA; ^pDepartment of Cardiology, Mayo Clinic, Rochester, Minn., USA; ^qDepartment of Nuclear Medicine, San Bortolo Hospital, Vicenza, Italy; ^rDepartment of Anesthesiology and Critical Care Medicine, Hôpital Lariboisière, University of Paris, Paris Diderot, France; ^sDepartment of Internal Medicine, University of Siena, Le Scotte Hospital, Siena, Italy; ^tDepartment of Anesthesiology, Duke University Medical Center, Durham, N.C., USA; ^uDepartment of Critical Care, University of Maryland, Baltimore, Md., USA; ^vDivision of Nephrology, Mediciti Hospitals, Hyderabad, India; ^wDepartment of Internal Medicine, San Bortolo Hospital, Vicenza, Italy; ^xDepartment of Intensive Care, San Bortolo Hospital, Vicenza, Italy; ^yCardiac Department, Faculty of Public Health, Medical University, Military Hospital, Wroclaw, Poland. ^*Author’s affiliation at the end of the article.

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Abstract

The cardiorenal syndrome (CRS) is a disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other. The general definition has been expanded into five subtypes reflecting the primacy of organ dysfunction and the time-frame of the syndrome: CRS type 1 = acute worsening of heart function leading to kidney injury and/or dysfunction; CRS type 2 = chronic abnormalities in heart function leading to kidney injury or dysfunction; CRS type 3 = acute worsening of kidney function leading to heart injury and/or dysfunction; CRS type 4 = chronic kidney disease leading to heart injury, disease and/or dysfunction, and CRS type 5 = systemic conditions leading to simultaneous injury and/or dysfunction of heart and kidney. Different pathophysiological mechanisms are involved in the combined dysfunction of heart and kidney in these five types of the syndrome.

Copyright © 2010 S. Karger AG, Basel

Combined heart and kidney dysfunction is common [1]. A disorder of one of these two organs often leads to dysfunction or injury to the other [2]. This is the pathophysiological basis for the clinical entity defined cardiorenal syndrome (CRS) [3]. Generally defined as a condition characterized by the initiation and/ or progression of renal insufficiency secondary to heart failure [4], the term CRS should also be used to describe conditions of renal dysfunction leading to heart dysfunction (renocardiac syndrome) [5]. The absence of a clear definition contributed in the past to a lack of clarity with regard to diagnosis and management [6]. The common view is that a relatively normal kidney is dysfunctional because of a diseased heart [7, 8]. This concept, however, has been challenged and the most recent definition includes a variety of conditions, either acute or chronic, where the primary failing organ can be either the heart or the kidney (table 1) [9]. Such advances in the definition and classification of CRS enabled the characterization of the complex organ crosstalk and have proposed specific prevention strategies and therapeutic interventions to attenuate end organ injury [5, 6, 10]. A major problem with previous terminology was that it did not allow identification of the pathophysiological interactions occurring in the different types of combined heart/kidney disorder [11]. The subdivision into different subtypes seems to provide a better approach to this syndrome.

Cardiorenal Syndrome Type 1 (Acute Cardiorenal Syndrome)

Type 1 or acute CRS is characterized by an acute heart disorder leading to acute kidney injury (AKI; fig. 1). Several patients are admitted to hospital with either de novo acute heart failure (AHF) or with an acute decompensated heart failure [12]. Among these patients, pre-morbid renal dysfunction is common and predisposes to AKI [13, 14]. In AHF, AKI seems to be more severe in patients with impaired left ventricular ejection fraction (LVEF) compared to those with preserved LVEF [15, 16]. Furthermore, impaired renal function is consistently found as an independent risk factor for 1-year mortality in AHF patients including patients with ST-elevation myocardial infarction [16, 17]. This independent effect might be due to an associated acceleration in cardiovascular pathobiology due to kidney dysfunction through the activation of inflammatory pathways [8, 18]. AKI induced by primary cardiac dysfunction implies inadequate renal perfusion until proven otherwise. This should prompt clinicians to consider the diagnosis of a low cardiac output state and/or marked increase in venous pressure leading to kidney congestion. In this condition diuretic responsiveness may decrease. The physiological phenomena of diuretic breaking [19] and post-diuretic sodium retention [20] may also play a role in this setting. AKI can also be worsened by the administration of diuretics at higher doses. Accordingly, diuretics may best be given in AHF patients with evidence of systemic fluid overload with the goal of achieving gradual diuresis. Furosemide can be titrated according to renal function, systolic blood pressure and monitoring of AKI biomarkers. A continuous diuretic infusion might be helpful [21]. In parallel, measurement of cardiac output, venous pressure and bioelectric impedance vector analysis may also help ensure continued and targeted diuretic therapy while preventing unwanted iatrogenic com...