Acute hypotension is a common complication of haemodialysis, occurring in 20-33% of patients in different series. Although the immediate cause is increasing intravascular hypovolaemia related to the dialysis procedure, no constant relationship exists between volume status or degree of volume loss and development of hypotension, emphasizing the importance of additional factors which render certain patients susceptible to this complication. These may include autonomic neuropathy, left ventricular hypertrophy (LVH) and diastolic dysfunction, inappropriate activation of cardiovascular reflexes, and abnormal vascular compliance. In contrast to earlier studies implicating autonomic neuropathy in intradialytic hypotension, recent reports have failed to confirm differences in autonomic function or baroreflex sensitivity in patients with and without hypotensive episodes. However, there is a strong association between LVH and dialysis hypotension. LVH is very common in ESRD, increases with time on dialysis, and is present in up to two-thirds of chronic dialysis patients. A close relationship exists between LVH and impaired diastolic relaxation, which is also common in ESRD patients. Patients prone to hypotension are characterized by both LVH and diastolic dysfunction, with an impaired early to late ventricular filling ratio, together with virtual complete cessation of passive ventricular filling prior to development of hypotension. Impaired cardiac filling and reduced cardiac output do not fully explain dialysis hypotension; in most subjects the response is reflex sympathetic activation and peripheral vasoconstriction, with maintenance of blood pressure. Syncope may result from activation of ventricular mechanoreceptor afferents as a response to left ventricular underfilling, with a resulting paradoxical withdrawal of sympathetic activity and of reflex vasoconstriction. Other potential factors increasing susceptibility to hypotension include impaired venous compliance, which predisposes to reduced venous return, seen particularly in elderly hypertensive and diabetic ESRD patients. Anaemia, inadequate vascular refilling rate, and overactivity of the NO vasodilator pathway have also been proposed to contribute to the pathogenesis of intradialytic hypotension. Excessive interdialytic weight gain is not directly related to hypotension, but EDTA data have shown it to be associated with increased cardiovascular mortality. Despite this, interdialytic weight gain is not related either to interdialytic blood pressure change, nor to development of LVH.