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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 148082, 8 pages
Review Article

Advances in the Pathogenesis of Cardiorenal Syndrome Type 3

1Department of Nephrology and Dialysis, San Giovanni Di Dio, Agrigento 92100, Italy
2Department of Nephrology, Dialysis and Transplant, San Bortolo Hospital, Vicenza 36100, Italy
3International Renal Research Institute Vicenza (IRRIV), Italy
4Clinical Genetics Unit, Department of Women’s and Children’s Health, University of Padua, Italy
5Department of Medicine (DIMED), University of Padova, Padova 35128, Italy
6Internal Medicine, San Bortolo Hospital, Vicenza 36100, Italy

Received 18 November 2014; Accepted 23 February 2015

Academic Editor: Ersin Fadillioglu

Copyright © 2015 Anna Clementi et al. 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.


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.