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Neurohormonal, Endocrine, and Immune Dysregulation and Inflammation in Cardiorenal Syndrome
Anna Clementi1,2, Grazia Maria Virzì3,4, Giovanni Giorgio Battaglia1
1Department of Nephrology and Dialysis, Santa Marta and Santa Venera Hospital, Acireale, Italy.
Insights
Cardiorenal syndrome (CRS) involves complex heart and kidney interactions. This review explores key mechanisms like inflammation and immune dysregulation in CRS development.
Area of Science:
- Physiology
- Pathology
- Cardiology
- Nephrology
Background:
- Organ crosstalk is vital for physiological balance.
- Cardiorenal syndrome (CRS) describes heart and kidney interactions in disease.
- CRS involves multifaceted pathophysiological processes.
Purpose of the Study:
- To review the complex mechanisms underlying cardiorenal syndrome (CRS).
- To focus on neurohormonal, endocrine, and immune dysregulation in CRS pathogenesis.
- To highlight inflammation's role in the development of CRS.
Main Methods:
- Literature review focusing on cardiorenal syndrome.
- Analysis of pathophysiological mechanisms in CRS.
- Synthesis of current understanding on organ crosstalk between heart and kidney.
Main Results:
- CRS involves intricate bidirectional communication between the heart and kidneys.
- Numerous factors contribute to CRS, including hemodynamic and cellular processes.
- Neurohormonal, endocrine, and immune pathways are central to CRS pathogenesis.
Conclusions:
- Understanding CRS mechanisms is crucial for managing heart and kidney diseases.
- Inflammation and dysregulation of key systems drive CRS.
- Further research into these pathways may reveal therapeutic targets for CRS.
Abstract:
"Organ crosstalk" is the complex physiological communication between different body systems, and it is necessary for the optimal equilibrium and functioning of the organism. In particular, heart and kidney function is tightly connected, and interplay between these two organs occurs through a vast array of dynamic and bidirectional mechanisms. The term cardiorenal syndrome (CRS) indicates an interaction between the heart and kidneys in acute and chronic disease settings. In all types of CRS, multiple pathophysiological processes are implicated in the initiation and progression of organ injury. In addition to hemodynamic parameters, endothelial injury, immunological imbalance, cell death, inflammatory cascades, oxidative stress, neutrophil migration, leukocyte trafficking, caspase-mediated apoptosis, extracellular vesicles, small noncoding RNAs, and epigenetics play pivotal roles in the development of CRS. In this review, we will focus on neurohormonal, endocrine, and immune dysregulation and inflammation as mechanisms involved in the pathogenesis of CRS.
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