Chronic kidney disease (CKD) preceding the development of renal failure, is independently associated with cardiovascular outcomes as explained by a number of mechanisms including haemodynamic and non-haemodynamic factors.[1-3] Our aim was to evaluate whether the relationship between CKD and left ventricular mass (LVM) occurs in a community sample and the extent to which this relationship depends on haemodynamic factors. In 418 randomly selected, non-diabetic participants from a community sample, 236 of whom were normotensive (NT), glomerular filtration rate was estimated (eGFR), [3] LVM and dimensions determined using echocardiography, and aortic BP assessed from applanation tonometry and SphygmoCor software.[4] Unadjusted means and proportions were compared by the large-sample z test and the χ2-statistic, respectively. Relationships were determined using multivariate regression analysis with adjustments for clinic BP (or alternative haemodynamic factors), age, sex, waist circumference, HbA1c, regular tobacco intake, regular alcohol intake, pulse rate and treatment for hypertension in the models. Aortic pulse wave velocity and high quality 24-hour BP values were available from 362 and 304 participants respectively. With adjustments for confounders (including clinic systolic BP), eGFR was associated with LVM index (LVMI) and LVM in excess of that predicted from stroke work (inappropriate LVM, LVMinappr) in the whole sample (LVMI: partial r = – 0.24, p<0.005; LVMinappr: partial r = – 0.33, p<0.0001) and in NT only (LVMI: partial r = – 0.30, p<0.01; LVMinappr: partial r = – 0.37, p<0.0001). Differences in LVMI and LVMinappr were noted in the eGFR range above 105 mls/min/1.73 m2) (p<0.0001 for differences in LVMinappr between upper two quartiles of eGFR). When replacing clinic BP with either aortic systolic BP, 24-hour BP, PWV, stroke work (for LVMI), LV end diastolic volume, or circumferential wall stress in the regression models, eGFR retained the strong association with LVMI (p<0.05 to <0.0005) and LVMinappr (p<0.0001 for all) and these effects were replicated in NT only. Therefore, strong relationships between early renal dysfunction and LVM occur at a community level irrespective of the presence of hypertension and independent of 24-hour and aortic BP, PWV, LV end diastolic volume, stroke work and wall stress. Non-haemodynamic factors appear to explain a considerable proportion of the relationship between early CKD and LV hypertrophy.[5]