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Kidney Week

Abstract: PO0439

Antioxidant Prevents Deleterious Heart-Kidney Cross-Talk in a Novel Experimental Model of Cardiorenal Syndrome due to Isolated Right Heart Failure

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Author

  • Farahmand, Firoozeh, Saint Louis University, Saint Louis, Missouri, United States
Background


Since recognition of CRS, most studies have investigated left heart failure and CRS due to isolated RVF is under recognized. However, renal dysfunction is an independent predictor of death and hospitalization in RVF. To examine experimental models of CRS improve our understanding of the pathophysiology of RV-Kidney interaction and enable us to explore new therapeutic modalities.

Methods

In a alkaloid (ALK) injection induced CRS in rats we investigated whether antioxidant prevents deleterious interactions of RV-Kidney in CRS. Rats were treated with an antioxidant, 1 wk pre & post-ALK injection. At 3 and 4 wks post-ALK injection, serial echocardiography was performed to monitor cardiac function. RV systolic pressure (RVSP), RV hypertrophy (RVH), RV function, RV levels of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSHPx) and lipid peroxidation (LPX) were measured. After sacrificing animals, hearts and kidneys were removed for histopathology.

Results

At 4 weeks , ALK-induced CRS resulted in increased mortality, RVSP, RVH, and LPX in RV myocardium accompanied RVF as well as the kidney. Antioxidant enzymes activities including SOD and GSHPx were decreased in RV and the kidney. Kidney histopathology with Periodic acid-Schiff (PAS) staining demonstrated tubular epithelial denudation, a marker of ATN that was not seen at 3 weeks post-ALK injection. This excludes renal toxicity of the alkaloid. Antioxidant treatment prevents not only ALK-induced CRS and decreased oxidative stress but also increased the SOD and GSHPx levels in the RV myocardium and the kidney.

Conclusion

A reduction in oxidative stress by antioxidant may explain the prevention of ALK-induced CRS. Thus, targeting oxidative stress may lead to the development of novel therapies for CRS and antioxidants as an adjuvant therapy may be beneficial .