Role of sodium and volume in the pathogenesis of hypertension in dialysis patients. Reflections on pathophysiological mechanisms.

Volume and sodium excess is the predominant factor in the pathogenesis of hypertension in dialysis patients. However, except for anephric patients, the relationship between volume status, blood pressure, and hemodynamics is not straightforward, but may vary between subgroups of patients. In general, the sensitivity of blood pressure to changes in the volume/sodium status appears to be increased in patients with end-stage renal disease. The blood pressure response to changes in the sodium/volume status may be influenced by disturbances in the activity of and response to various neurohumoral mechanisms, such as the renin-angiotensin and sympathetic nervous systems, Na-K-ATP-ase inhibitors, and the nitric oxide system. Regarding these aspects, there might be a parallel with salt-sensitive (essential) hypertension. Preliminary data showed a beneficial effect of sodium removal beyond changes in the volume status. Also of interest is the fact that prolonging dialysis time may improve blood pressure control without clear changes in the fluid status. It is hypothesized that a reduction in exchangeable sodium, by increased diffusive transport of sodium, in combination with increased removal of vasopressor substances, might be partly responsible for the observed blood pressure changes during long dialysis times. In conclusion, sodium and volume overload and neurohumoral factors coincide in the pathogenesis of hypertension in dialysis patients. Nevertheless, their exact relationship has not yet been elucidated and deserves further study.