Related Experiment Video
Updated: Jun 5, 2025
Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Inflammation and Arterial Stiffness as Drivers of Cardiovascular Risk in Kidney Disease
Lorenzo Lo Cicero1, Paolo Lentini2, Concetto Sessa3,4
1School of Nephrology, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Insights
Patients with chronic kidney disease (CKD) face higher cardiovascular risk due to uremic toxins causing arterial stiffening. Targeting vascular function may reduce this risk, offering a potential therapeutic avenue.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Vascular Biology
Background:
- Patients with chronic kidney disease (CKD) exhibit elevated cardiovascular (CV) risk.
- CV risk correlates inversely with glomerular filtration rate in CKD patients.
Purpose of the Study:
- To review mechanisms of vascular dysfunction in CKD.
- To examine the role of inflammation in CKD-related vascular complications.
- To discuss the vascular effects of nephrology drugs.
Main Methods:
- Literature review of uremic toxins and vascular effects.
- Analysis of data from models of mild and severe inflammation.
- Discussion of pharmacological interventions in CKD.
Main Results:
- Uremic toxins induce vascular inflammation and oxidative stress.
- These factors lead to endothelial dysfunction and arterial stiffening.
- Arterial stiffening contributes to increased risk of myocardial infarction and stroke in CKD.
Conclusions:
- Vascular dysfunction, driven by uremic toxins, contributes significantly to CV risk in CKD.
- Reducing arterial stiffness correlates with decreased CV risk in end-stage kidney disease.
- Vascular function represents a potential therapeutic target for mitigating CV risk in CKD.
Background:
Patients with chronic kidney disease (CKD) have an increased cardiovascular (CV) risk. The lower the glomerular filtration rate, the higher the CV risk.
Summary:
Current data suggest that several uremic toxins lead to vascular inflammation and oxidative stress that, in turn, lead to endothelial dysfunction, changes in smooth muscle cells' phenotype, and increased degradation of elastin and collagen fibers. These processes lead to both functional and structural arterial stiffening and explain part of the increased risk of acute myocardial infarction and stroke reported in patients with CKD. Considering that, at least in patients with end-stage kidney disease, the reduction of arterial stiffness is associated with a parallel decrease of the CV risk; vascular function is a potential target for therapy to reduce the CV risk.
Key Messages:
In this review, we explore mechanisms of vascular dysfunction in CKD, paying particular attention to inflammation, reporting current data in other models of mild and severe inflammation, and discussing the vascular effect of several drugs currently used in nephrology.
Related Concept Videos
01:18Hypertension and Regulation of Blood Pressure
01:30Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
01:25Antihypertensive Drugs: Direct Renin Inhibitors
01:22Heart Failure Drugs: Diuretics
01:30Antihypertensive Drugs: Angiotensin II Receptor Blockers