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      Case report: severe bradycardia, a reversible cause of “Cardio-Renal-Cerebral Syndrome”

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          Abstract

          Background

          Cardio-Renal Syndromes were first classified in 2008 and divided into five subtypes. The type 1 Cardio-Renal Syndrome (CRS) is characterized by acute decompensation of heart failure leading to acute kidney injury (AKI). Bradyarrhythmia was not mentioned in the classification as a cause for low cardiac output (CO) in type 1 CRS. Besides, CRS was not previously associated with central nervous system (CNS) injury despite the fact that cardiac, renal and neurological diseases can coexist.

          Case presentation

          We report the case of a 93-year old diabetic man who presented for obnubilation. He had a slow atrial fibrillation, was not hypotensive and was not taking any beta-blocker. He developed, simultaneously, during his hospitalization, severe bradycardia (<35 beats per minute), oligoanuria and further neurological deterioration without profound hypotension. An ECG revealed a complete atrioventricular (AV) block and all his symptoms were completely reversed after pacemaker insertion. His creatinine decreased progressively afterwards and at discharge, he was conscious, alert and well oriented.

          Conclusion

          Our case highlights the importance of an early recognition of low cardiac output secondary to severe bradyarrhythmia and its concurrent repercussion on the kidney and the brain. This association of the CRS with CNS injury-that we called “Cardio-Renal-Cerebral Syndrome”–was successfully treated with permanent pacemaker implantation.

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          Most cited references17

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          Cardiorenal syndrome.

          The term cardiorenal syndrome (CRS) increasingly has been used without a consistent or well-accepted definition. To include the vast array of interrelated derangements, and to stress the bidirectional nature of heart-kidney interactions, we present a new classification of the CRS with 5 subtypes that reflect the pathophysiology, the time-frame, and the nature of concomitant cardiac and renal dysfunction. CRS can be generally defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction of 1 organ may induce acute or chronic dysfunction of the other. Type 1 CRS reflects an abrupt worsening of cardiac function (e.g., acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type 2 CRS comprises chronic abnormalities in cardiac function (e.g., chronic congestive heart failure) causing progressive chronic kidney disease. Type 3 CRS consists of an abrupt worsening of renal function (e.g., acute kidney ischemia or glomerulonephritis) causing acute cardiac dysfunction (e.g., heart failure, arrhythmia, ischemia). Type 4 CRS describes a state of chronic kidney disease (e.g., chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy, and/or increased risk of adverse cardiovascular events. Type 5 CRS reflects a systemic condition (e.g., sepsis) causing both cardiac and renal dysfunction. Biomarkers can contribute to an early diagnosis of CRS and to a timely therapeutic intervention. The use of this classification can help physicians characterize groups of patients, provides the rationale for specific management strategies, and allows the design of future clinical trials with more accurate selection and stratification of the population under investigation.
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            Cardiorenal syndrome type 1: pathophysiological crosstalk leading to combined heart and kidney dysfunction in the setting of acutely decompensated heart failure.

            Cardiorenal syndrome (CRS) type 1 is characterized as the development of acute kidney injury (AKI) and dysfunction in the patient with acute cardiac illness, most commonly acute decompensated heart failure (ADHF). There is evidence in the literature supporting multiple pathophysiological mechanisms operating simultaneously and sequentially to result in the clinical syndrome characterized by a rise in serum creatinine, oliguria, diuretic resistance, and in many cases, worsening of ADHF symptoms. The milieu of chronic kidney disease has associated factors including obesity, cachexia, hypertension, diabetes, proteinuria, uremic solute retention, anemia, and repeated subclinical AKI events all work to escalate individual risk of CRS in the setting of ADHF. All of these conditions have been linked to cardiac and renal fibrosis. In the hospitalized patient, hemodynamic changes leading to venous renal congestion, neurohormonal activation, hypothalamic-pituitary stress reaction, inflammation and immune cell signaling, systemic endotoxemic exposure from the gut, superimposed infection, and iatrogenesis all contribute to CRS type 1. The final common pathway of bidirectional organ injury appears to be cellular, tissue, and systemic oxidative stress that exacerbate organ function. This review explores in detail the pathophysiological pathways that put a patient at risk and then effectuate the vicious cycle now recognized as CRS type 1. Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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              The evaluation and management of bradycardia.

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                Author and article information

                Contributors
                aounmabel@yahoo.fr
                randa_22tabbah@hotmail.com
                Journal
                BMC Nephrol
                BMC Nephrol
                BMC Nephrology
                BioMed Central (London )
                1471-2369
                26 October 2016
                26 October 2016
                2016
                : 17
                : 162
                Affiliations
                [1 ]Nephrology Department of Saint-Georges Hospital Ajaltoun and Saint-Joseph University, Beirut, Lebanon
                [2 ]Holy Spirit University of Kaslik, Jounieh, Lebanon
                Author information
                http://orcid.org/0000-0001-9893-5514
                Article
                375
                10.1186/s12882-016-0375-7
                5081674
                ac7a019b-7cc2-45fb-b9e0-1788bae6f62e
                © The Author(s). 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 17 May 2016
                : 18 October 2016
                Categories
                Case Report
                Custom metadata
                © The Author(s) 2016

                Nephrology
                cardio-renal syndrome,acute kidney injury,low cardiac output,bradyarrhythmia,neurological deterioration,pacemaker,case report

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