Cardiovascular (CV) disease is the main cause of morbidity and mortality in dialysis patients. Hypertension in patients affected by chronic renal insufficiency (CRI) has been recognized as one of the major classical CV risk factors in CRI from the very beginning of the dialysis era. However, its treatment is still unsatisfactory. A discussion is employed to achieve a consensus on key points relating to the epidemiological, pathophysiological and clinical characteristics of hypertension in renal patients, in the light of global CV risk assessment. CV disease is accelerated by CRI, in particular by uraemia-specific risk factors. This is reflected by the fact that general population-based equations for calculating CV risk underestimate the real CV risk in CRI and dialysis patients. Hypertension in dialysis patients is clearly a major CV risk factor. Isolated systolic hypertension with increased pulse pressure is the most prevalent blood pressure (BP) anomaly in dialysis patients, due to stiffening of the arterial tree. BP should be assessed by clinical measurements on a routine basis, leaving 24 h monitoring for selected cases. The targets of BP control should be those recommended by the present guidelines, i.e. <140/90 mmHg, or the lowest possible values that are well tolerated. The pathophysiological cornerstone of hypertension in dialysis patients is extra-cellular volume expansion, which is typically sodium-sensitive, given the loss of renal function. Therefore, the principles of hypertension treatment in dialysis are an achievement of dry body weight, proper dialysis prescription with respect to dialysis time and intra-dialytic sodium balance, and dietary sodium and water restriction. Pharmacological treatment should only be the second option, after the adequate and complete application of all other means. No comparative pharmacological trials have specifically addressed the issue of hypertension control in dialysis patients. Therefore, this workshop group had to rely largely on data obtained in the general population. Drugs interfering with the renin-angiotensin system were felt to be the first choice, as they have widely been shown to interfere significantly with CV remodelling. Despite long-standing concerns, beta-blockers are being used increasingly even in patients with congestive heart failure and ischaemic cardiomyopathy. Other drug classes may be used in association or as first-line agents according to clinical requirements. Hypertension in renal patients has to be given particular and continued attention, and it should be adequately treated in light of the increased CV risk of this patient population. Research into the mechanisms of uraemic cardiomyopathy and cardiovascular remodelling should provide a precious new insight and lead to more precisely targeted and more effective therapies than in the past.
