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Updated: Dec 3, 2025

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Endothelial dysfunction and cardiovascular risk in lupus nephritis: New roles for old players?
Daniele Mancardi1, Elisa Arrigo1, Martina Cozzi2,3
1Department of Clinical and Biological Sciences, University of Torino, Torino, Italy.
Insights
Systemic lupus erythematosus (SLE) and lupus nephritis (LN) involve endothelial dysfunction, impacting cardiovascular health. Understanding these vascular changes is key to developing targeted treatments for SLE and LN patients.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Immunology
Background:
- Systemic lupus erythematosus (SLE) and lupus nephritis (LN) are characterized by endothelial dysfunction, contributing to cardiovascular complications.
- Kidney damage in LN can negatively impact the cardiovascular system, increasing risks for hypertension and stroke.
Purpose of the Study:
- To review the literature on endothelial activation and dysfunction in SLE and LN patients.
- To explore similarities and differences in arteriovenous endothelial pathways and microcirculation versus macrocirculation.
- To identify potential therapeutic targets for cardiovascular complications in SLE and LN.
Main Methods:
- Comprehensive literature review of recent studies on endothelial dysfunction in SLE and LN.
- Analysis of arteriovenous endothelial cell activation pathways.
- Comparison of microcirculation and macrocirculation manifestations.
Main Results:
- Endothelial dysfunction is a shared vascular component in SLE clinical manifestations and LN.
- Kidney damage in LN exacerbates cardiovascular risk factors.
- Specific pathways in venous versus arterial endothelial cells and microcirculation versus macrocirculation require further elucidation.
Conclusions:
- Critical summary of current data on endothelial dysfunction in SLE/LN is vital for developing new treatments.
- Further research into arteriovenous differences and micro/macrocirculation is needed.
- Targeting endothelial dysfunction may offer novel therapeutic strategies for cardiovascular complications in SLE and LN.
Abstract:
In systemic lupus erythematosus (SLE) patients, most of the clinical manifestation share a vascular component triggered by endothelial dysfunction. Endothelial cells (ECs) activation occurs both on the arterial and venous side, and the high vascular density of kidneys accounts for the detrimental outcomes of SLE through lupus nephritis (LN). Kidney damage, in turn, exerts a negative feedback on the cardiovascular (CV) system aggravating risk factors for CV diseases such as hypertension, stroke and coronary syndrome among others. Despite the intensive investigation on SLE and LN, the role of endothelial dysfunction, as well as the underlying mechanisms, remains to be fully understood, with no specifically targeted pharmacological treatment. It is not known, in fact, if the activation pathway(s) in venous ECs are similar to the one in arterial ECs and doubts persist on the shared manifestation of microcirculation compared to macrocirculation. In this work, we aim to review the recent literature about the role of endothelial activation and dysfunction in the development of CV complications in SLE and LN patients. We, therefore, focus on arteriovenous similarities and differences and on specific pathways of great vessels compared to capillaries. Critically summarising the available data is of pivotal importance for both basic researchers and clinicians in order to develop and test new pharmacological approaches in the treatment of basic components of SLE and LN.
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