Table 3. Studies explicating the importance of oxidative stress in cardiorenal syndrome (CRS) type I pathophysiology.

RAS- renin-angiotensin system, SNS- sympathetic nervous system, ESRD- end stage renal disease, MPO- myeloperoxidase

AUTHOR & YEAR OF PUBLICATION	TYPE OF STUDY & # OF PATIENTS	PURPOSE OF STUDY	CONCLUSION
Lullo et al. [2] 2017	Review	Update on the pathophysiology of CRS types 1-5	To elucidate the burden of pathophysiology in CRS types 1-5 on the functioning of the heart and kidney.
Virzì et al. [5] 2014	Review	The Hemodynamic and Non-hemodynamic Cross-talk in CRS type I	To elaborate molecular, cellular, and subcellular features for advancing treatments.
McCullough [13] 2011	Review	Cardiorenal syndrome: pathophysiology to prevention	Importance of catalytic iron in organ injury and other biomarkers for diagnosis, treatment, and prognosis.
Bongartz et al. [16] 2004	Review	The severe Cardiorenal syndrome: Guyton Revisited	To unravel the harmful consequences of RAS, RNS &ROS, inflammation, and SNS.
Virzì et al. [39] 2018	In vitro study, 53 patients	Levels of Pro-inflammatory cytokines, oxidative stress, and tissue damage markers in patients with acute heart failure with and without CRS type I	High levels of Pro-inflammatory cytokines, oxidative stress, and biomarkers are the crux of CRS type I pathophysiology.
Virzì et al. [42] 2015	In vitro study, 23 patients	Oxidative stress: Dual Pathway Induction in CRS Type I Pathogenesis	To understand the imbalances of reactive oxygen species and nitrogen species in CRS type I and their implications in activating the inflammatory cascade.
Maruyama et al. [43] 2004	Review	Inflammation and oxidative stress in ESRD-the role of myeloperoxidase	Inflammation increases cardiovascular risk in end-stage renal disease. Furthermore, MPO associated oxidative stress is a significant risk factor for vascular dysfunction.