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Updated: Mar 21, 2026
Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
The Validity of Left Ventricular Mass as a Surrogate End Point for All-Cause and Cardiovascular Mortality Outcomes in
Sunil V Badve1, Suetonia C Palmer2, Giovanni F M Strippoli3
1Australasian Kidney Trials Network, Brisbane, Australia; School of Medicine, The University of Queensland, Brisbane, Australia; Department of Nephrology, St. George Hospital, Sydney, Australia; The George Institute for Global Health, University of Sydney, Sydney, Australia.
Insights
Left ventricular mass (LVM) reduction is often used in chronic kidney disease (CKD) trials. However, this study found no clear link between LVM changes and mortality, questioning its use as a surrogate endpoint in CKD.
Area of Science:
- Cardiology
- Nephrology
- Clinical Trials
Background:
- Left ventricular mass (LVM) reduction is a common surrogate endpoint in chronic kidney disease (CKD) research.
- It is assumed that reducing LVM lowers cardiovascular risk in CKD patients.
Purpose of the Study:
- To evaluate the validity of LVM as a surrogate endpoint for all-cause and cardiovascular mortality in individuals with CKD.
- To determine if changes in LVM accurately predict mortality outcomes.
Main Methods:
- A systematic review and meta-analysis of randomized controlled trials (RCTs) involving CKD participants.
- Included trials had at least 3 months of follow-up and reported LVM data.
- Analyzed 73 trials with 6,732 participants across 25 intervention classes.
Main Results:
- Only three interventions demonstrated a reduction in LVM: erythropoiesis-stimulating agents, renin-angiotensin-aldosterone system inhibitors, and isosorbide mononitrate.
- All interventions showed uncertain effects on all-cause and cardiovascular mortality.
- Weak and imprecise associations were found between LVM changes and both all-cause and cardiovascular mortality.
Conclusions:
- The current evidence does not support a clear association between intervention-induced LVM change and mortality outcomes in CKD.
- The validity of LVM as a surrogate endpoint for mortality in CKD is currently lacking due to limited data and study quality.
- Further research with high-quality, long-term data is needed to clarify the role of LVM in CKD clinical trials.
Background:
Left ventricular mass (LVM) is a widely used surrogate end point in randomized trials involving people with chronic kidney disease (CKD) because treatment-induced LVM reductions are assumed to lower cardiovascular risk. The aim of this study was to assess the validity of LVM as a surrogate end point for all-cause and cardiovascular mortality in CKD.
Study Design:
Systematic review and meta-analysis.
Setting & Population:
Participants with any stages of CKD.
Selection Criteria For Studies:
Randomized controlled trials with 3 or more months' follow-up that reported LVM data.
Intervention:
Any pharmacologic or nonpharmacologic intervention.
Outcomes:
The surrogate outcome of interest was LVM change from baseline to last measurement, and clinical outcomes of interest were all-cause and cardiovascular mortality. Standardized mean differences (SMDs) of LVM change and relative risk for mortality were estimated using pairwise random-effects meta-analysis. Correlations between surrogate and clinical outcomes were summarized across all interventions combined using bivariate random-effects Bayesian models, and 95% credible intervals were computed.
Results:
73 trials (6,732 participants) covering 25 intervention classes were included in the meta-analysis. Overall, risk of bias was uncertain or high. Only 3 interventions reduced LVM: erythropoiesis-stimulating agents (9 trials; SMD, -0.13; 95% CI, -0.23 to -0.03), renin-angiotensin-aldosterone system inhibitors (13 trials; SMD, -0.28; 95% CI, -0.45 to -0.12), and isosorbide mononitrate (2 trials; SMD, -0.43; 95% CI, -0.72 to -0.14). All interventions had uncertain effects on all-cause and cardiovascular mortality. There were weak and imprecise associations between the effects of interventions on LVM change and all-cause (32 trials; 5,044 participants; correlation coefficient, 0.28; 95% credible interval, -0.13 to 0.59) and cardiovascular mortality (13 trials; 2,327 participants; correlation coefficient, 0.30; 95% credible interval, -0.54 to 0.76).
Limitations:
Limited long-term data, suboptimal quality of included studies.
Conclusions:
There was no clear and consistent association between intervention-induced LVM change and mortality. Evidence for LVM as a valid surrogate end point in CKD is currently lacking.
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