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Cardiorenal syndrome: pathophysiological mechanism, preclinical models, novel contributors and potential therapies
Qiang Fu1, Longxing Cao1, Huang Li2
1Cardiovascular Division, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, China.
Insights
Cardiorenal syndrome involves heart and kidney failure, where one organ
Area of Science:
- Cardiorenal Medicine
- Nephrology
- Cardiology
Background:
- Cardiorenal syndrome (CRS) is a complex condition where heart and kidney dysfunction exacerbate each other, leading to progressive organ failure.
- The pathophysiology of CRS is multifactorial, involving neurohormonal activation, endothelial dysfunction, proteinuria, oxidative stress, and uremic toxins.
- Current management of CRS presents significant therapeutic challenges due to the opposing effects of treatments on cardiac and renal functions.
Purpose of the Study:
- To review current knowledge on the pathophysiological mechanisms of cardiorenal syndrome.
- To explore preclinical models, contributing factors, and potential therapeutic strategies for cardiorenal syndrome.
- To highlight the need for better disease models and therapeutic targets in cardiorenal syndrome management.
Main Methods:
- Literature search of PubMed for articles on cardiorenal syndrome published in English up to January 2014.
- Selection and analysis of original articles and critical reviews related to cardiorenal syndrome.
- Synthesis of current understanding regarding CRS pathophysiology, contributors, and therapeutic challenges.
Main Results:
- Cardiorenal syndrome is characterized by the mutual worsening of heart and kidney failure.
- Potential pathophysiological contributors include neurohormonal activation, endothelial dysfunction, proteinuria, oxidative stress, and uremic toxins.
- Non-dialyzable uremic toxins, such as indoxyl sulfate, demonstrate detrimental cardiac and renal effects and may represent a therapeutic target.
Conclusions:
- There is an urgent need for suitable preclinical models to investigate cardiorenal syndrome pathophysiology and therapies.
- Targeting non-dialyzable protein-bound uremic toxins may offer therapeutic benefits for patients with cardiorenal syndrome.
- Further research into the complex interplay between cardiac and renal systems is crucial for effective cardiorenal syndrome management.
Objective:
To review the current knowledge about the pathophysiological mechanisms, preclinical models, novel contributors and potential therapies of cardiorenal syndrome.
Data Sources:
The literature concerning cardiorenal syndrome in this review was collected from PubMed published in English up to January 2014.
Study Selection:
Original articles and critical reviews related to cardiorenal syndrome were selected and carefully analyzed.
Results:
Cardiorenal syndrome is a condition characterized by kidney and heart failure where failure of one organ worsens the function of the other thus further accelerating the progressive failure of both organs. The pathophysiology of cardiorenal syndrome is not fully understood, but may be caused by a complex combination of neurohormonal system activation, endothelial dysfunction, proteinuria, oxidative stress, uremic toxins and other factors. Managing cardiorenal syndrome is still a major therapeutic challenge in clinical practice because many of the drugs used to control heart failure can worsen renal function, and vice versa. Non-dialyzable uremic toxins, such as indoxyl sulfate, causing detrimental effects on the heart and kidney as well as stimulation of inflammatory responses, may be an effective therapeutic target for cardiorenal syndrome.
Conclusions:
Suitable disease models of cardiorenal syndrome are urgently needed to investigate the pathophysiology and effective therapeutic approaches to the condition. Non-dialyzable protein-bound uremic toxins that may have cardiac and renal effects may provide therapeutic benefit to cardiorenal syndrome patients.
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