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Updated: May 31, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Allopurinol benefits left ventricular mass and endothelial dysfunction in chronic kidney disease
Michelle P Kao1, Donald S Ang, Stephen J Gandy
1Division of Medical Sciences, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, United Kingdom. mpckao@doctors.org.uk
Insights
Allopurinol significantly reduced left ventricular hypertrophy (LVH) and improved endothelial function in patients with chronic kidney disease (CKD). These findings suggest allopurinol may offer cardiovascular benefits for this population.
Area of Science:
- Cardiology
- Nephrology
- Pharmacology
Background:
- Allopurinol is known to improve endothelial function and arterial stiffness in non-CKD patients.
- The effects of allopurinol on cardiovascular parameters in patients with chronic kidney disease (CKD) remain unclear.
- Arterial stiffness contributes to left ventricular hypertrophy (LVH) by increasing afterload.
Purpose of the Study:
- To investigate the efficacy of allopurinol in reducing LVH and improving endothelial function in patients with stage 3 CKD.
- To assess the impact of allopurinol on arterial stiffness in this patient cohort.
Main Methods:
- A randomized, double-blind, placebo-controlled, parallel-group study.
- 67 patients with stage 3 CKD and LVH were assigned to receive either allopurinol (300 mg/d) or placebo for 9 months.
- Left ventricular mass index (LVMI) was measured by cardiac MRI, endothelial function by flow-mediated dilation (FMD), and arterial stiffness by pulse-wave analysis.
Main Results:
- Allopurinol significantly reduced LVH (P=0.036).
- Allopurinol significantly improved endothelial function (P=0.009).
- Allopurinol significantly improved the central augmentation index, a measure of arterial stiffness (P=0.015).
Conclusions:
- Allopurinol treatment effectively regresses left ventricular mass and enhances endothelial function in patients with CKD.
- Given the association of LVH and endothelial dysfunction with poor prognosis, these findings warrant further investigation into allopurinol's potential to reduce cardiovascular events in CKD patients.
Abstract:
Allopurinol ameliorates endothelial dysfunction and arterial stiffness among patients without chronic kidney disease (CKD), but it is unknown if it has similar effects among patients with CKD. Furthermore, because arterial stiffness increases left ventricular afterload, any allopurinol-induced improvement in arterial compliance might also regress left ventricular hypertrophy (LVH). We conducted a randomized, double-blind, placebo-controlled, parallel-group study in patients with stage 3 CKD and LVH. We randomly assigned 67 subjects to allopurinol at 300 mg/d or placebo for 9 months; 53 patients completed the study. We measured left ventricular mass index (LVMI) with cardiac magnetic resonance imaging (MRI), assessed endothelial function by flow-mediated dilation (FMD) of the brachial artery, and evaluated central arterial stiffness by pulse-wave analysis. Allopurinol significantly reduced LVH (P=0.036), improved endothelial function (P=0.009), and improved the central augmentation index (P=0.015). This study demonstrates that allopurinol can regress left ventricular mass and improve endothelial function among patients with CKD. Because LVH and endothelial dysfunction associate with prognosis, these results call for further trials to examine whether allopurinol reduces cardiovascular events in patients with CKD and LVH.
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