In the past, it had been presumed that hypertension in chronic renal diseas
e can be explained by the dual effects of sodium retention and inappropriat
e activity of the renin-angiotensin system. Recent experimental and clinica
l data provide strong evidence that the increase in blood pressure is to a
large part due to sympathetic overactivity which is triggered by afferent s
ignals emanating from the kidney and resetting sympathetic tone by stimulat
ion of hypothalamic centres. The sequelae of sympathetic overactivity exten
d beyond their effects on blood pressure and include accelerated progressio
n of renal failure and presumably increased cardiac arrhythmia.