The dialyzer has the unique ability to control directly the extracellular volume (ECV). Therefore blood pressure (BP) can be controlled by dialysis alone . At the same time, antihypertensive medications are all but useless in dialysis patients . Furthermore, failure to stop these medications when beginning to lower the ECV makes it impossible to use this method . Lack of understanding of these basic principles may explain why hypertension (HT) is so poorly controlled. We shall review succinctly how to control BP in the dialysis patient.

In the early 70's although hemodialysis (HD) technique was still basic and antihypertensive therapy rudimentary, HT was controlled in 90% of HD patients . Twenty years later BP control has worsen, the prevalence of HT in big series has reached 80% of patients . This is all the more paradoxical as we have today the tools we lacked in the late 60's: for ECV estimation (inferior vena cava diameter, bioimpedance, ANP, GMP,...), as for continuous ultrafiltration (UF) and dialysate sodium control.

The most obvious consequence of the poor HT control is that cardiovascular (CV) morbidity remains by far the first cause of death and that we are facing a real epidemic of CV disease in HD patients. A shocking reality, especially as in non uremic patients Framingham and other studies have demonstrated a clear reduction of CV morbidity and mortality along years by controlling HT.

Which are the causes of this poor HT control on dialysis today? Can we expect any improvement? Addressing these questions requires considering two possible complementary explanations: lack of interest for volume control and difficulty to achieve it.

Are some nephrologists poorly motivated? Who really cares for hypertension ? Several reasons may have lead to neglect hypertension control as a critical factor of clinical outcome.

Questionable benefit of controlling HT? Some reports show a better survival in hypertensive compared to normotensive HD patients . Indeed, such reports are based on short-term (a few years) observation whereas the effect of HT in reducing mortality takes as much as 10 years to be observed .

Hypotension per se may carry a higher risk than HT . The correlation of hypotension (essentially diastolic) with early mortality is explained in great part by the fact that it is a marker of poor CV status (congestive heart failure) or frailty preceding death .

The "U curve" phenomenon reported in uremic as in non uremic patients reflects therefore the association of an increased early mortality in hypotensive patients with an increased long-term mortality in hypertensive patients. There is no contradiction. That hypotension is a marker of high short-term mortality does not exclude that HT is a powerful risk factor for long-term mortality, and it must be treated as such.

A second reason for the nephrology community to have neglected HT control is that the Kt/V concept has focused all the interest, the dose being considered the only "key to survival" . In fact HD outcome does not need a single one, but several conditions. Small and middle molecule clearances, nutrition, ECV and BP control are so far well identified factors. Each and any of these factors if lacking leads to poor clinical outcome even if the others are fulfilled. Furthermore, the dose of dialysis is independent of BP control. Some groups achieve a good BP control with a just "adequate" Kt/V . At opposite, providing a large dose of dialysis does not insure good BP control .

Did we forget how to manage BP by extracellular volume (ECV)control?

This may arise first from conceptual difficulties.

The poor terminology used in fluid and electrolyte balance (e.g., using the term of "dehydration" to mean saline depletion, or "hyperhydratation" to mean saline excess) is a source of confusion. It may explain why patients are so often asked to reduce their fluid intake, whereas it is the salt which must be restricted. The efficiency of sodium restriction (i.e. ECV reduction) in controlling HT has been established in essential hypertension , as in dialysis . After the first decade of dialysis, it has been almost forgotten. Its value has been recently re-emphasized in association with lower dialysate sodium.

The great point with the dry weight concept is that it relates two universally available simple, easily measurable values, weight and blood pressure, to define the adequate ECV. "It is the average level of sodium in the body over a long period of time that correlates with blood pressure". Unfortunately there is/has been a frequent misunderstanding of what the dry weight really is. Dry weight is not the actual but the ideal post-dialysis weight of a patient, the one that achieves normotension and normal volume state. Another common confusion is made between dry weight and interdialytic weight change, and number of reports have based on the poor correlation between interdialytic weight change and BP their affirmation that BP in dialysis is not/poorly linked to ECV.

Another possibility is that there is now a real increasing difficulty in evaluating or achieving DW.

Do we have difficulty because clinical evaluation of DW is a poor method? Several authors have claimed that it is uneasy, unreliable and inaccurate. But the method was good enough to permit a control of HT in 90% of HD patients in the 60’s, as it still does in some units . The many substitution tools for ECV "objective" assessment have not proven their superiority over the clinical method in everyday practice, and these units reporting excellent BP control use nothing else than the clinical determination of DW. Clinical evaluation of dry weight (DW) is a time consuming task which must be performed very regularly but it is not a difficult task. It must include collection of simple but mandatory data such as clinical story, neck vein reading, or cardiothoracic ratio on x-ray. In case of doubt on the DW value one may return to the "probe" method, systematical, step-by-step progressive lowering (or increasing) of the post-dialysis weight over some weeks until a normal stable BP is achieved and maintained.

Practical difficulties in achieving DW may rise from too short a HD session. The good results in ECV and BP control are achieved mostly using long dialysis or a daily dialysis . These methods have in common that they allow for a reduction of ECV with a low rate of intradialytic morbidity as well as the interruption of all antihypertensive medications. Because they potentiate hypotensive episodes during ultrafiltration antihypertensive medications are one of the strongest barriers to achieving dry weight .

It is fair to add that recently published data show that using a short thrice-weekly dialysis schedule does not prevent to control HT without antihypertensive medication if a low salt diet is used together with a reasonably low (138 mmol/L) dialysate sodium . This opens a brand new field of investigation on improvement of the presently "conventional" HD method. On the other hand, the changing case mix of patients (increasing age, proportion of diabetic and cardiovascular compromised patients) has to be considered, and the more physiological forms of treatment (long slow or daily HD) probably will be needed to face this changing situation.

Altogether, control of hypertension should be refocused as an essential target of dialysis today. We may have underestimated the importance of the goal, misunderstood the theory and practice of ECV control. It is time to get back to the dry weight method. It should reduce the very high incidence of cardiovascular events, which presently burden the dialysis population. If implemented, reasonable sodium dialysate concentration, low salt diet, sufficiently long or frequent HD sessions to improve the UF tolerance, but more than anything else, the determination of the nephrologists should suffice to achieve this goal.