Dear Colleagues,

The term “Cardiorenal Syndrome” (CRS) includes a scenario of clinical interactions in which cardiac and renal dysfunction coexist. The crosstalk between the heart and the kidney has been clearly established but not fully understood. Many different factors have been shown to be involved in the pathogenesis of CRS. Mechanisms leading to CRS are multi-factorial and involve not only hemodynamic parameters.
Recently, considerable attention has been paid to the role of new alternative mechanisms which may be implicated in the pathogenesis of cardiorenal crosstalk, such as epigenetics, prenatal programming, small non-coding RNA and extracellular vesicles, and their possible role in heart and kidney disease.
Acute kidney injury develops in CRS type 1 due to a rapid worsening of cardiac function, whereas in CRS type 3 it is responsible for acute cardiac damage. In CRS type 5, acute kidney injury and cardiac dysfunction coexist in the setting of systemic disorders, such as sepsis, autoimmune disease and diabetes mellitus. Beyond hemodynamic pathways, other mechanisms have been described to be involved in the pathogenesis of all these syndromes, including the activation of the sympathetic nervous system, innate and adaptive immunity dysregulation, inflammation and impaired balance of reactive oxygen species (ROS) versus nitric oxide (NO) production.
In this Special Issue, we invite original research as well as review articles giving high priority to the following topics:
- Different types of Cardiorenal Syndrome
- Pathophysiology of Cardiorenal Syndrome
- Molecular and cellular mechanisms underlying Cardiorenal Syndrome
- Hemodynamic and non-hemodynamic mechanisms in Cardiorenal Syndrome
- Organ crosstalk between heart and kidney

Dr. Grazia Maria Virzì and Dr. Anna Clementi
Guest Editors