03162nas a2200289   4500000000100000008004100001260001700042100001400059700001400073700001400087700001700101700001500118700001500133700001200148700001300160700001600173700001700189700001300206700001500219700002200234700001900256245017700275250001500452490003300467520232100500020005102821       2016                            d  c1695200111831 aHawley C.1 aPascoe E.1 aPalmer S.1 aStrippoli G.1 aRoberts M.1 aJohnson D.1 aCass A.1 aCraig J.1 aHiremath S.1 aBoudville N.1 aBadve S.1 aWhalley G.1 aTeixeira-Pinto A.1 aPerkovic Vlado00aThe Validity of Left Ventricular Mass as a Surrogate End Point for All-Cause and Cardiovascular Mortality Outcomes in People With CKD: A Systematic Review and Meta-analysis  a2016/05/040 vpii: S0272-6386(16)30024-5. 3 a<p>
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 &amp; 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.
</p>
  a1523-6838 (Electronic)<br/>0272-6386 (Linking)