In patients with end-stage renal disease (ESRD), at the time they start dialysis HBP is common and has been attributed to volume overload or an active RAS (10). Early in the history of hemodialysis the potential for the RAS to be involved in causing HBP was unclear, but studies with saralasin (11,12), a competitive angiotensin II antagonist, clearly showed that in dialysis patients with elevated plasma renin levels the renin was involved in causing HBP by leading to the generation of angiotensin II. Although a number of other mechanisms apart from volume and angiotensin II have been considered, there is little evidence today that any, including aldo, play a regular role in causing HBP in the dialysis setting.