Recent studies considered that an increase in sympathetic activity (SA) may be responsible for left ventricular hypertrophy (LVH). Before and after renal transplantation (RT), we evaluated changes on left ventricular mass (LVM) and SA in 40 end-stage renal disease patients between 8 and 35 years old. Hypertension (95.0% vs. 71.0%; p=0.005), use of combined antihypertensive drugs (57.5% vs. 30.0%; p=0.01), and LVH (77.5% vs. 52.5%; p=0.01) significantly decreased after RT whereas low-to-high frequency ratio (LF/HF), which represents SA, increased (3.1 vs. 5.3; p=0.0001). However, LVM regressors (with decrease on LVM index more than 20%) showed a trend of lower change on LF/HF ratio (1.6 vs. 2.4; p= 0.09) than nonregressors. Living-donor graft, baseline LVM, use of antihypertensive drugs, lower change on LF/HF ratio, and lower systolic blood pressure levels were associated with LVM regression in the simple correlation analysis. However, in the logistic regression analysis, only baseline LVM and donor type remained in the model (R(2)=0.35; p=0.0003). Thus, LVH decreased after RT and was related to baseline LVM and living-donor type. However, it is possible that the higher persistence of LVH after RT could be explained at least in part by increase in heart sympathetic activity and use of immunosuppressors.