Background-Uremia is proposed to increase sympathetic nerve activity (SNA) in hemodialysis patients. The aims of the present study were to determine whether reversal of uremia by successful kidney transplantation (RTX) eliminates the increased SNA and whether signals arising in the diseased kidneys contribute to the increased SNA in renal failure. Methods and Results-We compared muscle sympathetic nerve activity (MSNA) in 13 hemodialysis patients wait-listed for RTX and in renal transplantation patients with excellent graft function treated with cyclosporine (RTX-CSA, nϭ13), tacrolimus (RTX-FK, nϭ13), or without calcineurin inhibitors (RTX-Ø, nϭ6), as well as in healthy volunteers (CON, nϭ15). In addition to the above patients with present diseased native kidneys, we studied 16 RTX patients who had undergone bilateral nephrectomy (RTX-NE). Data are meanϮSEM. MSNA was significantly elevated in hemodialysis patients (43Ϯ4 bursts/min), RTX-CSA (44Ϯ5 bursts/min), RTX-FK (34Ϯ3 bursts/min), and RTX-Ø (44Ϯ5 bursts/min) as compared with CON (21Ϯ3 bursts/min), despite excellent graft function after RTX. RTX-NE had significantly reduced MSNA (20Ϯ3 bursts/min) when compared with RTX patients. MSNA did not change significantly with RTX in 4 hemodialysis patients studied before and after RTX (44Ϯ6 versus 43Ϯ5 bursts/min, PϭNS). In contrast, nephrectomy resulted in reduced MSNA in all 6 RTX patients studied before and after removal of the second native kidney. Conclusions-Despite correction of uremia, increased SNA is observed in renal transplant recipients with diseased native kidneys at a level not significantly different from chronic hemodialysis patients. The increased SNA seems to be mediated by signals arising in the native kidneys that are independent of circulating uremia related toxins. (Circulation.
The greater efficacy of lacidipine on carotid IMT progression and number of plaques per patient, despite a smaller ambulatory blood pressure reduction, indicates an antiatherosclerotic action of lacidipine independent of its antihypertensive action.
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