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Updated: Jun 21, 2026
Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Effect of spironolactone on left ventricular mass and aortic stiffness in early-stage chronic kidney disease: a
Nicola C Edwards1, Richard P Steeds, Paul M Stewart
1Department of Cardiology, University Hospital Birmingham and University of Birmingham, Birmingham, UK.
Insights
Adding spironolactone to standard treatments significantly reduces left ventricular mass and improves arterial stiffness in early-stage chronic kidney disease (CKD) patients. This suggests spironolactone
Area of Science:
- Nephrology and Cardiovascular Medicine
- Pharmacology of Aldosterone Antagonists
Background:
- Chronic kidney disease (CKD) is linked to increased cardiovascular disease (CVD) risk.
- Left ventricular hypertrophy and arterial stiffness are common in CKD, indicating poor prognosis.
- Renin-angiotensin-aldosterone system (RAAS) activation is implicated in these cardiovascular abnormalities.
Purpose of the Study:
- To evaluate if spironolactone improves cardiac and vascular health in early CKD.
- To assess the impact of adding spironolactone to ACE inhibitors (ACEi) or angiotensin receptor blockers (ARBs) in CKD patients.
Main Methods:
- 112 patients with stage 2-3 CKD and controlled blood pressure on ACEi/ARBs participated.
- Patients underwent a run-in phase with spironolactone, then were randomized to continue spironolactone or placebo for 40 weeks.
- Left ventricular mass (cardiac MRI) and arterial stiffness (pulse wave velocity, aortic distensibility) were measured.
Main Results:
- Spironolactone significantly reduced left ventricular mass compared to placebo.
- Significant improvements were observed in pulse wave velocity and augmentation index.
- Aortic distensibility also showed significant improvement with spironolactone treatment.
Conclusions:
- Spironolactone effectively reduces left ventricular mass and arterial stiffness in early CKD.
- These findings suggest aldosterone has detrimental cardiovascular effects in CKD.
- Spironolactone warrants further investigation for preventing adverse cardiovascular events in CKD.
Objectives:
We sought to determine whether the addition of spironolactone to angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) improves left ventricular mass and arterial stiffness in early-stage chronic kidney disease (CKD).
Background:
Chronic kidney disease is associated with a high risk of cardiovascular disease and a high prevalence of left ventricular hypertrophy and arterial stiffness that confer an adverse prognosis. It is believed that these abnormalities are in part a result of activation of the renin-angiotensin-aldosterone system.
Methods:
After an active run-in phase with spironolactone 25 mg once daily, 112 patients with stage 2 and 3 CKD with good blood pressure control (mean daytime ambulatory blood pressure <130/85 mm Hg) on established treatment with ACE inhibitors or ARBs were randomized to continue spironolactone or to receive a matching placebo. Left ventricular mass (cardiac magnetic resonance) and arterial stiffness (pulse wave velocity/analysis, aortic distensibility) were measured before run in and after 40 weeks of treatment.
Results:
Compared with placebo, the use of spironolactone resulted in significant improvements in left ventricular mass (-14 +/- 13 g vs. +3 +/- 11 g, p < 0.01), pulse wave velocity (-0.8 +/- 1.0 m/s vs. -0.1 +/- 0.9 m/s, p < 0.01), augmentation index (-5.2 +/- 6.1% vs. -1.4 +/- 5.9%, p < 0.05), and aortic distensibility (0.69 +/- 0.86 x 10(-3) mm Hg vs. 0.04 +/- 1.04 x 10(-3) mm Hg, p < 0.01).
Conclusions:
The use of spironolactone reduces left ventricular mass and improves arterial stiffness in early-stage CKD. These effects suggest that aldosterone exerts adverse cardiovascular effects in CKD and that spironolactone is worthy of further study as a treatment that could reduce adverse cardiovascular events. (Is Spironolactone Safe and Effective in the Treatment of Cardiovascular Disease in Mild Chronic Renal Failure; NCT00291720).
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