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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 391790, 9 pages
http://dx.doi.org/10.1155/2015/391790
Research Article

Oxidative Stress: Dual Pathway Induction in Cardiorenal Syndrome Type 1 Pathogenesis

1Department of Nephrology, Dialysis and Transplant, San Bortolo Hospital, 36100 Vicenza, Italy
2International Renal Research Institute of Vicenza (IRRIV), Italy
3Department of Nephrology and Dialysis, San Giovanni Di Dio Hospital, 92100 Agrigento, Italy
4Department of Medicine DIMED, University of Padua Medical School, 35128 Padua, Italy
5Laboratory of Experimental Hepatology, Department of Medicine, University of Padua, 35128 Padua, Italy
6Department of Information Engineering, University of Padua, 35128 Padua, Italy
7Internal Medicine, San Bortolo Hospital, 36100 Vicenza, Italy
8Internal Medicine Unit, Sant’Antonio Hospital, 35127 Padua, Italy

Received 3 December 2014; Revised 11 February 2015; Accepted 15 February 2015

Academic Editor: Noriko Noguchi

Copyright © 2015 Grazia Maria Virzì 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.

Abstract

Cardiorenal Syndrome Type 1 (Type 1) is a specific condition which is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Even though its pathophysiology is complex and not still completely understood, oxidative stress seems to play a pivotal role. In this study, we examined the putative role of oxidative stress in the pathogenesis of CRS Type 1. Twenty-three patients with acute heart failure (AHF) were included in the study. Subsequently, 11 patients who developed AKI due to AHF were classified as CRS Type 1. Quantitative determinations for IL-6, myeloperoxidase (MPO), nitric oxide (NO), copper/zinc superoxide dismutase (Cu/ZnSOD), and endogenous peroxidase activity (EPA) were performed. CRS Type 1 patients displayed significant augmentation in circulating ROS and RNS, as well as expression of IL-6. Quantitative analysis of all oxidative stress markers showed significantly lower oxidative stress levels in controls and AHF compared to CRS Type 1 patients (). This pilot study demonstrates the significantly heightened presence of dual oxidative stress pathway induction in CRS Type 1 compared to AHF patients. Our findings indicate that oxidative stress is a potential therapeutic target, as it promotes inflammation by ROS/RNS-linked pathogenesis.