Background: Chronic kidney disease (CKD) patients often have sympathetic hyperactivity, which contributes to the pathogenesis of hypertension and cardiovascular organ damage. Angiotensin-converting enzyme (ACE) inhibitors (ACEi) and angiotensin II receptor blockers (ARB) reduce sympathetic hyperactivity. Ideally, treatment should eliminate the relation between sympathetic activity and organ damage. The aim of the present study is firstly to compare left ventricular mass (LVM) of CKD patients using chronic ACEi or an ARB with LVM of controls. Secondly, we determine whether previously found muscle sympathetic nerve activity (MSNA) and arterial blood pressure during follow-up are predictive for the presence of increased LVM. Methods. We restudied 20 CKD patients and 30 healthy volunteers matched for age. Sympathetic nerve activity was quantified by the microneurography (MSNA). Arterial blood pressure was the mean of office blood pressure measurements. LVM was quantified by magnetic resonance imaging (MRI) without contrast.
Results: The period between MSNA and MRI measurements was 9 ± 3 years. All patients were treated according to guidelines with an ACEi or an ARB. In CKD patients, mean systolic and diastolic arterial pressure were 129 ± 10 and 84 ± 5 mmHg, respectively, during follow-up. In patients, as compared to controls, LVM was 93 ± 16 versus 76 ± 18 g, LVM index 30 ± 5 versus 24 ± 4 g/m(2.7) and mean wall thickness 11 ± 2 versus 9.0 ± 1 mm (all P < 0.01). Moreover, MSNA was related to LVM (r = 0.65, P < 0.002), LVM index (r = 0.46, P < 0.03) and LV mean wall thickness (r = 0.84, P < 0.001). Conclusions. In conclusion, the present study demonstrates that measures of LVM in CKD patients are greater than in healthy controls, despite a well-controlled blood pressure in the patients. Moreover, there is a positive relationship between these measures of LVM and MSNA, assessed years before, despite a standard antihypertensive treatment. These results support the notion that additional sympatholytic therapy could be beneficial.