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Review
. 2015:2015:148082.
doi: 10.1155/2015/148082. Epub 2015 Mar 4.

Advances in the pathogenesis of cardiorenal syndrome type 3

Anna Clementi  1 , Grazia Maria Virzì  2 , Alessandra Brocca  3 , Massimo de Cal  4 , Silvia Pastori  4 , Maurizio Clementi  5 , Antonio Granata  1 , Giorgio Vescovo  6 , Claudio Ronco  4
Affiliations
Review

Advances in the pathogenesis of cardiorenal syndrome type 3

Anna Clementi et al. Oxid Med Cell Longev. 2015.

Abstract

Cardiorenal syndrome (CRS) type 3 is a subclassification of the CRS whereby an episode of acute kidney injury (AKI) leads to the development of acute cardiac injury or dysfunction. In general, there is limited understanding of the pathophysiologic mechanisms involved in CRS type 3. An episode of AKI may have effects that depend on the severity and duration of AKI and that both directly and indirectly predispose to an acute cardiac event. Experimental data suggest that cardiac dysfunction may be related to immune system activation, inflammatory mediators release, oxidative stress, and cellular apoptosis which are well documented in the setting of AKI. Moreover, significant derangements, such as fluid and electrolyte imbalance, metabolic acidosis, and uremia, which are typical features of acute kidney injury, may impair cardiac function. In this review, we will focus on multiple factors possibly involved in the pathogenesis issues regarding CRS type 3.

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Figures

Figure 1
Figure 1
Direct mechanism of cardiorenal syndrome type 3.
See this image and copyright information in PMC

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