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The Cardiorenal Syndrome: Making the Connection

The heart and the kidneys share responsibility for maintaining hemodynamic stability and end-organ perfusion. Connections between these organs ensure that subtle physiologic changes in one system are tempered by compensation in the other through a variety of pathways and mediators. In the setting of...

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Detalles Bibliográficos
Autores principales: Viswanathan, Gautham, Gilbert, Scott
Formato: Texto
Lenguaje:English
Publicado: SAGE-Hindawi Access to Research 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989717/
https://www.ncbi.nlm.nih.gov/pubmed/21151533
http://dx.doi.org/10.4061/2011/283137
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author Viswanathan, Gautham
Gilbert, Scott
author_facet Viswanathan, Gautham
Gilbert, Scott
author_sort Viswanathan, Gautham
collection PubMed
description The heart and the kidneys share responsibility for maintaining hemodynamic stability and end-organ perfusion. Connections between these organs ensure that subtle physiologic changes in one system are tempered by compensation in the other through a variety of pathways and mediators. In the setting of underlying heart disease or chronic kidney disease, the capacity of each organ to respond to perturbation caused by the other may become compromised. This has recently led to the characterization of the cardiorenal syndrome (CRS). This review will primarily focus on CRS type 1 where acute decompensated heart failure (ADHF) results in activation of hemodynamic and neurohormonal factors leading to an acute drop in the glomerular filtration rate and the development of acute kidney injury. We will examine the scope and impact of this problem, the pathophysiology associated with this relationship, including underperfuson and venous congestion, diagnostic tools for earlier detection, and therapeutic interventions to prevent and treat this complication.
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spelling pubmed-29897172010-12-13 The Cardiorenal Syndrome: Making the Connection Viswanathan, Gautham Gilbert, Scott Int J Nephrol Review Article The heart and the kidneys share responsibility for maintaining hemodynamic stability and end-organ perfusion. Connections between these organs ensure that subtle physiologic changes in one system are tempered by compensation in the other through a variety of pathways and mediators. In the setting of underlying heart disease or chronic kidney disease, the capacity of each organ to respond to perturbation caused by the other may become compromised. This has recently led to the characterization of the cardiorenal syndrome (CRS). This review will primarily focus on CRS type 1 where acute decompensated heart failure (ADHF) results in activation of hemodynamic and neurohormonal factors leading to an acute drop in the glomerular filtration rate and the development of acute kidney injury. We will examine the scope and impact of this problem, the pathophysiology associated with this relationship, including underperfuson and venous congestion, diagnostic tools for earlier detection, and therapeutic interventions to prevent and treat this complication. SAGE-Hindawi Access to Research 2010-10-04 /pmc/articles/PMC2989717/ /pubmed/21151533 http://dx.doi.org/10.4061/2011/283137 Text en Copyright © 2011 G. Viswanathan and S. Gilbert. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Viswanathan, Gautham
Gilbert, Scott
The Cardiorenal Syndrome: Making the Connection
title The Cardiorenal Syndrome: Making the Connection
title_full The Cardiorenal Syndrome: Making the Connection
title_fullStr The Cardiorenal Syndrome: Making the Connection
title_full_unstemmed The Cardiorenal Syndrome: Making the Connection
title_short The Cardiorenal Syndrome: Making the Connection
title_sort cardiorenal syndrome: making the connection
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989717/
https://www.ncbi.nlm.nih.gov/pubmed/21151533
http://dx.doi.org/10.4061/2011/283137
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