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Updated: Dec 29, 2025

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Epicardial Adipose Tissue, Adiponectin and Leptin: A Potential Source of Cardiovascular Risk in Chronic Kidney
Luis D'Marco1, Maria Jesús Puchades1, Jose Luis Gorriz1
1Nephrology Department, Hospital Clínico Universitario, INCLIVA, University of Valencia, 46010 Valencia, Spain.
Insights
Epicardial adipose tissue (EAT) significantly impacts cardiovascular disease risk, especially in chronic kidney disease (CKD) patients. EAT influences atherosclerosis via adipokines like adiponectin and leptin, highlighting its role in cardiometabolic health.
Area of Science:
- Cardiology
- Nephrology
- Endocrinology
Background:
- Cardiovascular disease (CVD) is highly prevalent in chronic kidney disease (CKD) patients.
- Factors beyond diabetes and metabolic syndrome contribute to this increased CVD risk.
- Visceral adipose tissue, particularly epicardial adipose tissue (EAT), is implicated in atherosclerosis.
Purpose of the Study:
- To review the impact of EAT on cardiovascular outcomes.
- To explore EAT's role in both the general population and CKD patients.
- To examine adiponectin and leptin as mediators of EAT-associated cardiovascular risk.
Main Methods:
- Literature review of current knowledge on EAT and cardiovascular outcomes.
- Focus on studies investigating EAT in general and CKD populations.
- Analysis of adipocytokines (adiponectin, leptin) secreted by EAT.
Main Results:
- EAT is increasingly recognized as a significant cardiometabolic factor.
- EAT influences atherosclerosis through paracrine and endocrine pathways.
- Adiponectin and leptin are key adipocytokines involved in EAT's effects.
Conclusions:
- EAT plays a crucial role in promoting atherosclerosis and cardiovascular complications.
- EAT's impact is particularly relevant in the context of chronic kidney disease.
- Adiponectin and leptin are potential mediators linking EAT to elevated cardiovascular risk.
Abstract:
The importance of cardiometabolic factors in the inception and progression of atherosclerotic cardiovascular disease is increasingly being recognized. Beyond diabetes mellitus and metabolic syndrome, other factors may be responsible in patients with chronic kidney disease (CKD) for the high prevalence of cardiovascular disease, which is estimated to be 5- to 20-fold higher than in the general population. Although undefined uremic toxins are often blamed for part of the increased risk, visceral adipose tissue, and in particular epicardial adipose tissue (EAT), have been the focus of intense research in the past two decades. In fact, several lines of evidence suggest their involvement in atherosclerosis development and its complications. EAT may promote atherosclerosis through paracrine and endocrine pathways exerted via the secretion of adipocytokines such as adiponectin and leptin. In this article we review the current knowledge of the impact of EAT on cardiovascular outcomes in the general population and in patients with CKD. Special reference will be made to adiponectin and leptin as possible mediators of the increased cardiovascular risk linked with EAT.
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