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Published on: December 2, 2016
Cardiac Remodeling in Chronic Kidney Disease
Nadine Kaesler1, Anne Babler1, Jürgen Floege1
1Clinic for Renal and Hypertensive Disorders, Rheumatological and Immunological Disease, University Hospital of the RWTH Aachen, 52074 Aachen, Germany.
Insights
Chronic kidney disease (CKD) severely impacts heart health through cardiorenal crosstalk, leading to cardiac remodeling and failure. This review explores mechanisms driving CKD-related heart disease and potential therapeutic targets.
Area of Science:
- Nephrology
- Cardiology
- Pathophysiology
Background:
- Chronic kidney disease (CKD) is linked to significant cardiac remodeling, impacting patient quality of life and survival.
- Existing treatments for CKD-related cardiac dysfunction are insufficient.
- The decline in kidney function disrupts metabolic pathways, affecting the heart via organ crosstalk.
Purpose of the Study:
- To review established and potential pathophysiological mechanisms of cardiorenal crosstalk in CKD.
- To identify how uremia-induced senescence and disease progression affect cardiac function.
- To explore potential therapeutic targets and relevant animal models for understanding and treating these conditions.
Main Methods:
- Literature review of established and potential pathophysiological cardiorenal crosstalk mechanisms.
- Analysis of factors contributing to cardiac remodeling in CKD patients.
- Examination of animal models for insights into disease progression and therapeutic strategies.
Main Results:
- CKD involves numerous factors like altered hemodynamics, metabolic disturbances, uremic toxins, and inflammation that stress the heart.
- These factors lead to left-ventricular hypertrophy, fibrosis, capillary rarefaction, and heart failure.
- Fibrosis in the heart contributes to electrical instability and sudden cardiac death.
Conclusions:
- Cardiorenal crosstalk is a critical driver of cardiac disease in CKD.
- Understanding these mechanisms is essential for developing novel therapeutics.
- Further research using animal models may elucidate new treatment strategies for uremia-induced cardiac pathology.
Abstract:
Cardiac remodeling occurs frequently in chronic kidney disease patients and affects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart functions are highly connected by organ crosstalk. Among others, altered volume and pressure status, ischemia, accelerated atherosclerosis and arteriosclerosis, disturbed mineral metabolism, renal anemia, activation of the renin-angiotensin system, uremic toxins, oxidative stress and upregulation of cytokines stress the sensitive interplay between different cardiac cell types. The fatal consequences are left-ventricular hypertrophy, fibrosis and capillary rarefaction, which lead to systolic and/or diastolic left-ventricular failure. Furthermore, fibrosis triggers electric instability and sudden cardiac death. This review focuses on established and potential pathophysiological cardiorenal crosstalk mechanisms that drive uremia-induced senescence and disease progression, including potential known targets and animal models that might help us to better understand the disease and to identify novel therapeutics.
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