It has been suggested that the increase in blood pressure observed in transplant patients treated with cyclosporine is mediated by cyclosporine-induced sympathoexcitation. However, the chronic effects of cyclosporine on sympathetic outflow in renal transplant patients have not been investigated. Therefore we studied sympathetic nerve activity and blood pressure before and 6 months after the withdrawal of cyclosporine in renal transplant patients.Methods
Twenty-four renal transplant patients with histologically confirmed chronic allograft nephropathy (age 48 ± 3 years, 60 ± 10 months after transplantation) were included in the prospective study and randomly assigned to either withdrawal (n = 12) or continuation (n = 12) of cyclosporine. Both groups received mycophenolate mofetil and prednisolone as additional immunosuppressants. At entry and 6 months later blood pressure, muscle sympathetic nerve activity (MSNA), and plasma norepinephrine were measured. To assess the potential influence of the diseased native kidneys, three renal transplant patients who had their native kidneys removed were studied before and after cyclosporine withdrawal.Results
Mean arterial pressure decreased significantly in the cyclosporine-withdrawal group (95 ± 4 versus 105 ± 4 mmHg 6 versus 0 months, P < 0.05) but not in the cyclosporine-continuation group (103 ± 3 versus 105 ± 4 mmHg, NS). However, plasma norepinephrine and MSNA did not change significantly in either group (MSNA 43 ± 4 versus 44 ± 3 and 38 ± 5 versus 39 ± 4 bursts/min in the cyclosporine-withdrawal and cyclosporine-continuation groups, NS). Graft function remained stable in both groups and in transplant patients who had their native kidneys removed MSNA did not decrease after cyclosporine withdrawal.Conclusion
The withdrawal of cyclosporine in renal transplant patients, receiving relatively low doses of cyclosporine, resulted in a substantial decrease in blood pressure. However, MSNA and norepinephrine did not change. This suggests that cyclosporine treatment does not cause chronic sympathetic activation that could explain the cyclosporine-induced blood pressure elevation in renal transplant patients.