Muscle sympathetic nerve does not decrease early after renal transplantation

Abstract

Uremia is proposed to cause tonic activation of the sympathetic nervous system in hemodialysis patients (HD) which may contribute to the high cardiovascular morbidity and mortality in this population. The effect of renal transplantation (RTX) with correction of uremia has not yet been investigated. Therefore, we compared muscle sympathetic nerve activity (MSNA) in HD wait-listed for RTX, in renal allograft recipients 3 months after transplantation treated with cyclosporine (RTX-CSA) or tacrolimus (RTX-FK) and in healthy volunteers (CTR) matched for age, sex, body mass index and time since onset of end-stage renal disease (RTX and HD). Exclusion criteria were diabetes mellitus and clinical evidence of atherosclerotic disease. We measured supine blood pressure (MAP, automatic sphygmomanometer), heart rate (HR, ECG), calf blood flow (plethysmography) and MSNA (microneurography) in the fasting state at least 12 hours after intake of any medication (HD and NTX) and calculated calf vascular resistance (CVR). (See Table) Data are mean ± SEM. p < 0.05 vs. CTR, p < 0.05 vs. HD(ANOVA, Fisher's PLSD). Data are mean ± SEM. p < 0.05 vs. CTR, p < 0.05 vs. HD(ANOVA, Fisher's PLSD). The results show increased muscle sympathetic nerve activity in both hemodialysis patients and renal allograft recipients as compared to healthy volunteers. Despite correction of uremia MSNA does not normalize in cyclosporine treated renal transplant patients early after transplantation.