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Cardiorenal Syndrome Revisited
Faiez Zannad1,2, Patrick Rossignol1,2,3
1Universite de Lorraine, Inserm, Centre d'Investigations Cliniques-1433 and Inserm U1116, CHRU Nancy, France (F.Z., P.R.).
Fibrosis, a common pathway in heart and kidney disease, may be the primary driver of cardiorenal syndromes. Targeting fibrosis could lead to new treatments for these interconnected conditions.
Area of Science:
- Cardiology
- Nephrology
- Pathophysiology
Background:
- Cardiorenal syndromes are classified into 5 subtypes, but this descriptive approach lacks pathophysiological insight and clinical impact.
- Existing classifications do not fully explain the complex interplay between cardiac and renal dysfunction.
- Recent research points to shared pathophysiological pathways underlying cardiorenal syndromes.
Purpose of the Study:
- To propose fibrosis as a unifying pathogenic mechanism in cardiorenal syndromes.
- To shift focus from descriptive classification to a mechanistic understanding of cardiorenal interactions.
- To identify fibrosis as a potential therapeutic target for cardiorenal conditions.
Main Methods:
- Review of current scientific literature on cardiorenal syndromes and fibrosis.
- Analysis of common pathophysiological pathways linking cardiac and renal diseases.
- Conceptualization of fibrosis as a central mediator in the cardiorenal syndrome continuum.
Main Results:
- Fibrosis is identified as a common consequence of inflammation and oxidative stress in conditions like aging, hypertension, and diabetes.
- Interstitial fibrosis is a prevalent feature in both heart failure and chronic kidney disease.
- Fibrosis is proposed as a potential primary driver, not just a marker, of cardiorenal pathophysiology.
Conclusions:
- Fibrosis may serve as a central pathogenic mechanism across various cardiorenal syndromes.
- Targeting fibrosis could offer a novel therapeutic strategy for cardiorenal conditions.
- Developing antifibrotic agents may revolutionize the prevention and treatment of cardiorenal syndrome.
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