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Updated: Aug 14, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
[Pro- and antiatherogenic mechanisms in chronic kidney failure]
Insights
Atherosclerosis accelerates in chronic renal insufficiency (ChRI) patients due to specific proatherogenic and antiatherogenic factors. Further research is needed to understand ChRI pathogenesis for better prevention and treatment.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Pathophysiology
Context:
- Atherosclerosis is a major cause of mortality in patients with chronic renal insufficiency (ChRI).
- Understanding the mechanisms driving accelerated atherosclerosis in ChRI is crucial for patient outcomes.
- Patients with manifest and terminal ChRI, undergoing various renal replacement therapies, are the focus.
Purpose:
- To review current knowledge on the causes of rapidly advancing atherosclerosis in chronic renal insufficiency.
- To discuss both generally known and ChRI-specific proatherogenic mechanisms.
- To explore antiatherogenic mechanisms relevant to chronic renal insufficiency.
Summary:
- This review examines the complex interplay of factors contributing to accelerated atherosclerosis in chronic renal insufficiency (ChRI).
- It details proatherogenic influences, including those unique to ChRI, and counteracting antiatherogenic mechanisms.
- The article synthesizes current understanding of atherosclerosis development in patients on conservative treatment, hemodialysis, or peritoneal dialysis.
Impact:
- Highlights the need for targeted research into ChRI pathogenesis.
- Suggests avenues for developing novel preventive and therapeutic strategies for atherosclerosis in renal insufficiency.
- Aims to improve clinical management and reduce mortality associated with cardiovascular complications in ChRI patients.
Abstract:
Atherosclerosis is a very common complication and frequently recordable cause of death in patients with chronic renal insufficiency (ChRI). The authors focus on current notions about causes of rapidly advancing atherosclerosis in patients presenting with manifest and terminal ChRI, who were exposed to a conservative treatment, programme hemodialysis or prolonged peritoneal dialysis. Treated in the article at length are proatherogenic (generally known, common in ChRI only) and antiatherogenic mechanisms. A worthwhile line of investigations is suggested to be designed to study ChRI pathogenesis and devise relevant preventive and curative measures.
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