Slide 1

Good morning Mr Chairman, Ladies and Gentlemen. We will talk about hemodynamic management of acute renal failure in intensive care patients during the next 2 or 3 hours.

Slide 2

You will find these lectures and also the two preceding lectures at NDT educational so some advert for our own journal online which you can freely access.

Slide 3

Now the overview of my talk will be that I will point to you that, as already pointed out by the previous speakers, that it is important to look at how these mechanisms are going to work and I will point out to you that the regulation of renal perfusion will be one of the factors that will drive indeed the idea that we have to intervene very early, especially if we’re talking about hemodynamic management of acute renal failure.
I will say something about the fluid status in ICU patients, first of all how we can evaluate that and secondly how we can correct after evaluation and third to conclude I will talk about vaso-active drugs.

Slide 4

Now, first of all let’s start with the basics. There are some facts in life that you cannot escape from. There is no discussion that this should be the print of a whale.

Slide 5

Well, one of the basic things in acute kidney injury is the fact that the normal autoregulation of the kidney is completely lost during acute renal failure and you can see that this is a post ischemia model in the rat where you can see that in function of the renal perfusion pressure which is in fact, as already pointed out the difference between the arterial and the venous pressure, you can see that in function of this renal perfusion pressure in the normal rats there is no change in the single nephron of the glomerular filtration rate, whereas in the post ischemic rats you can see that first of all glomerular filtration rate is much lower and is completely dependent upon the perfusion pressure. The reason for that is that the blood flow during this single nephron is completely normal or is completely un-independent of the renal perfusion pressure whereas in the ischemic rats it’s completely dependent upon the perfusion pressure.

Slide 6

The results of that is, of course, that the intraglomerular pressure is only slightly dependent upon the perfusion pressure, whereas in the post ischemic kidney it’s completely dependent upon your perfusion pressure and the reason for that is that, of course, there is something going on which the capillary sphincters the pre and the post glomerulus sphincter being that in the normal rats as perfusion pressure goes up you will see that the vasodilation in the efferent vessel and that there will be vasoconstriction in the afferent vessel. Of course, Professor Ronco has pointed out to you that there might be differences between post-ischemic and the septic model but I remind you that these sphincters are activated by the endothelial function and that of course, also in septic patients or animals this endothelial function will be severely disturbed either by post-ischemia or either by inflammatory markers, so I’m quite confident but I have to be honest there’s no data in septic models as far as I know but I’m quite confident that the same principal of a complete loss of autoregulation will also be present in patients or in animals with sepsis. You can see this in a more graphic way presented here that in normal animals you have between a certain frame a complete maintenance of perfusion  pressure and relative renal blood flow, whereas in the post ischemia models this is a complete relation which are perfusion pressure.

Slide 7

So in fact the basic lesson is that if you want to alter hemodynamic management of our patients, the major aim should be to maintain the perfusion pressure of our kidney. If we want to maintain perfusion pressure what we need, of course, is a heart that will contract to put forward the volume. You will need the volume because it’s no use that the heart is contracting, if there is no volume present to be ejected and of course, the third factor there will be the size of the vessels yes or no being in vasodilation or in vasoconstriction. So we will talk about vasoconstrictive agents at the end.

Slide 8

First of all, the fluid status in intensive care patients. How do we assess that? It’s very clear that there is much reason to think that we can be very much astray when we’re talking about fluid status in intensive care patients. There is no problem if the patient is what I call dry-dry. If the patient, if you look at the crumbles into --- is completely dehydrated, he has been lying on the ground for 5 days without any access to food or drink, well, there is no reason to doubt that this patient will be dehydrated and will need fluids. There is no reason to think that if a patient has pleural effusions and has oedema all over the place and has crackles and reels and whatever that this patient is clearly fluid overloaded but however, we know that most of our patients are either wet-dry or dry-wet. The wet-dry patients are those with cardiac insufficiency where the pump is not working and for that reason the fluid is everywhere but not where it should be and it means that we either have to dehydrate these patients by diuretic therapy and thereby, causing the kidney to feel or to think that this patient is dehydrated or this patient has a cardial insufficiency and there is renal hypoperfusion because the pump is not working and for the kidney the effect is the same there is no perfusion of the kidney, so in view of the kidney there is dehydration of the patient. Whereas in contrast, if we’re talking about the dry-wet patient, well, this is of course, the typical picture of a septic patient where there is a lot of third spacing the risk of oedema all over the place but the fluid is not in the circulation and if there is no fluid in the circulation well, the heart cannot pump it out and there will be no blood pressure and there will be no perfusion.

Slide 9

So, the estimation of the fluid status, the functional fluid status of your patient is of extreme importance. Fortunately, there are some very elegant tests that you can use to ascertain that the fluid status of your patient is really as you can think of it. One of these things is a clinical test where we use the leg raising of the patient. Now, this has been taught to me 20 years ago by my former Professor of intensive care and I was very pleased to see in this issue of 2006 of Critical Care Medicine that now there is evidence based to prove that this technique indeed works because how is the experiment going, you see here the patient and then there is leg raising and you see in some patients there is no effect on the heart and blood flow change whereas, in some patients there is a change, an increase in fact, in aortic blood flow.

Slide 10

Then in a second phase of the study they infused some extra saline in these patients and you can see that in the patients who did not respond primary to this leg raising exercise, well they did not also respond to the fluid filling status. Whereas, the patients who did respond to the leg raising, they also responded to the fluid loading. So this is a trick that you can use in clinical circumstances indeed to see whether if you infuse volume into this patient, there will be a reaction in part of the aortic output, aortic blood flow increasing also the probability that you will be improving perfusion of your organs in -- the kidney and of course the reason why we have to be cautious not to inject fluid in all patients is that if you have an anuric patient and you instill fluid there might be an increased risk of RDS or pulmonary oedema present so you can first test this with this test. You can see that the receiver operating characteristics of this test are quite high. You can see that if you measure only the peripheral blood pressure well, it’s not that sensitive, there are some problems but if you really measure aortic blood flow and you can easily do that with an ultrasound of the echocardiography, so there is no problem and you can see that there is a very high sensitivity and specificity present in this very cheap and very gentle test.

Slide 11

What about the measure of the blood pressure in our patients? There has been a debate in the intensive care literature yes or no to use the radial versus the femoral blood pressure, some people advocating that the femoral blood pressure far better represents the systemic pressure than the radial artery. Well you can see clearly in this Bland-Altman analysis comparing radial versus femoral blood pressure that indeed both are very close and that there is no reason why you should change from the radial to the femoral artery as a measurement point for your peripheral blood pressure in intensive care patients.

Slide 12

What about the use of pulmonary artery catheters to assess volume status in our patients? Well, you can see first of all and this is a study published in New England very recently 2006, where they compared the outcome in patients treated with a pulmonary artery catheter as compared to patients where the only monitoring device was a central venous catheter and you can see that the outcome was not different between the catheter group and the pulmonary artery group and also the people who remained off ventilation was quite not different between the group using the pulmonary artery catheter and the central venous catheter. The only difference being that of course there were far more complications with the catheters in the pulmonary artery catheter group as compared to the CVC group. There was a slightly higher increase even in need for RRT in the pulmonary artery catheter group which might be related to the fact that probably less fluids were given to these patients because there was some doubt about the fluid status not being too high in the pulmonary artery catheter group but overall the conclusion of this study was that you can indeed monitor patients as good with a central venous catheter as with a pulmonary artery catheter.

Slide 13

Now there are some other measurements that we can accomplish to a certain volume status, at least from the point of view of the kidney to see whether the volume status of our patients yes or no is what we call in a prerenal state. Of course we all know that the urinary osmolarity, the urinary plasma creatinine ratio, the low urinary sodium excretion because we know that if you have acute tubular necrosis, as already pointed out by Claudio Ronco, there is a loss of polarity and our tubular cells will start to secrete actively sodium inside of the urine. So if you have a high urinary sodium, this might be a sign that there is something wrong already and that you’re not in the prerenal phase anymore but already in the failure phase, in the acute tubular necrosis phase. The only problem with sodium and also with the fractional excretion of sodium is of course the use of diuretics. If you use diuretics, well there might be a false increase in the fractional excretion of sodium and this might blur your vision on what’s really going on. Therefore, we advocate the use of the fractional excretion of urea which would be lower than 35% to talk about prerenal failure. The fact that urea is reabsorbed is, of course, an anti-diuretic hormone induced phenomenon.

Slide 14

In this study you can clearly see that if you use the cut-off of fractional excretion of sodium in patients with prerenal acute renal failure and on diuretics, that you will have a false positive diagnosis of ATN in a not indiscernible amount of patients, whereas if you use the fractional excretion of urea as a criterion, even in the patients on diuretics you will see that you will not have false positive effects. This might explain to my opinion partly the negative impact of diuretics because if you’re using diuretics, some people might think that they have a high sodium excretion and that there’s acute tubular necrosis and for that reason they will already start renal replacement therapy at a stage where the patient might still be in the region of the prerenal phase and can gain by simple hydration.

Slide 15

Now, once you have ascertained the hemodynamic status of your patients, and you think that there might be a problem with fluids in these patients, is it safe just to put in as much fluid as you can? It’s not because you think that in circulation, in the vascular space there is a lack of fluid, in the kidney it is sensed that there is less perfusion, a lack of perfusion in the kidney that it might help or be beneficial to try to restore that with fluid. What we’ve seen in this study and it has already been pointed out that as a part of the Yegenaga study you can see that in patients who were included in this study the first day of sepsis and one of the inclusion criteria was that they should have a normal renal function on the first day of sepsis and then their renal function was followed up after that inclusion.

Slide 16

And what you see in these patients is that already on the first day of sepsis even with a normal renal function those who will develop renal failure later on had a lower diuresis as compared to those who will not develop acute renal failure later on.

Slide 17

More important if you look at the patients who will later on develop acute renal failure, you can see that despite the fact that they had far more colloid fluid loading, far more fluid loading well they still developed acute renal failure, whereas in the no acute renal failure developing patients despite the fact that they had lower fluid loading they still did not develop acute renal failure.

Slide 18

If you look at the central venous pressure in these patients, you can see that already on the first day of sepsis, even at the moment that the kidney function was still normal, these patients had a higher central venous pressure as compared to those who later on will not develop acute renal failure. So these patients had already so-called between brackets a better fluid status, they received more fluids and despite that they still developed acute renal failure.

Slide 19

So this points to me that some patients, especially septic patients, fluid loading might not be useful and might even be dangerous because if you look at the oxygen in these patients, in spite oxygen percentage, you can see that the oxygen need was higher in the patients who developed acute renal failure later on as compared to the patients who did not develop acute renal failure later on.

Slide 20

This study has been on the screen also already before and this is probably because there is cross-talk between the kidney and the lungs and if the kidney is damaged even if you cannot see it on the serum creatinine on the first day of sepsis there is already something going on in the lungs meaning that there is a reduced expression of acquaporin 5 and that there is an overexpression of sodium channels also in the lungs making these patients prone that if you fluid load them, they will also develop acute respiratory distress syndrome or at least they will need more oxygen and even mechanical ventilation. So it might not be very suitable in these patients to fluid load them blindly just to restore their hemodynamic status.

Slide 21

Now if you decide to fluid load these patients, should you try to give as much as possible or should we rather be somewhat restrictive? Well, from this slide you can see and this study was also published in New England 2006 you can see they compared a liberal regimen of fluid regimen to a conservative restrictive fluid loading regimen and you can see that as regards to AKI, so acute kidney injury 3 days there was no difference the only difference being that in the conservative group there was a higher need or there was a higher implementation of renal replacement therapy.

Slide 22

Now, you can say that this is a disadvantage but if you look at what happened to these patients, well, in the conservative strategy the survival of the patients was better as compared to the liberal strategy and this might probably be related to the fact that in the patients who were on the conservative strategy less of them were needing mechanical ventilation. This points to the fact that if you have to choose between the kidney and the lungs, well and we have to be proud of ourselves here that we are better in replacing the kidney than our intensivists are in replacing the lung function.

Slide 23

So we have to choose and we have to make a choice there and I think we should rather go for a more restrictive fluid balance at least if we’re not sure that this is a real prerenal state and we will be able to mend the situation by applying more fluids inside of these patients.

Slide 24

So, we tried to evaluate hemodynamically how the fluid status of the patient was. We decided that there is lack of fluid. Which types of fluid are we going to give to try to restore the damage done in these patients? Well, the big debate has always been albumin colloids versus crystalloids saline. In this -- study, the SAFE study published in New England 2 years ago you can clearly see that the probability of survival was completely the same in the albumin versus the saline group. Of course, as saline is far less expensive it is clear that we should prefer to use saline over albumin in these patients.

Slide 25

Then you can say yes but in a septic patient there’s already some ARDS developing., should it not be more safe in these patients to use albumin? Well you can see that overall you’ve seen the data there was no difference but both in trauma as in severe sepsis, as in patients with ARDS the study was not able to show that there was a superior outcome with the expensive albumin as compared to the very inexpensive saline loading. So, I think yes, this is very good evidence that we should use crystalloids and not colloids in these patients.

Slide 26

The only important point and already pointed out by the previous speakers is the timing of your intervention and you can see here in the left panel what the effect is of hemodynamic intervention in patients after the onset of tissue hypoxia. You can see that the effect is zero, nada, nothing whereas if you try to improve your tissue perfusion by changing the hemodynamic status of your patients before organ damage has been done, you can see that the -- effect of course is positive and that indeed you can be able to restore the organ function in these patients pointing once again to the fact that the terminology of intensive care really points to the care that you point to the patients, the timing that you’re on the bedside of the patient and that you can react really at the moment that something is going wrong.

Slide 27

Now, once you’ve decided to restore hemodynamically the status of your patient, which goals should you aim at? Should we try to be conservative, 65 mmHg of mean arterial pressure defined as 2 times diastolic, 1 times systolic divided by 3? Or should we go to 85 mmHg? Well, in this study you can see that in both regimens there is no difference in urine flow, there is no difference in serum creatinine level, there is no difference in creatinine clearance, there is no difference in oxygen delivery between the conservative and the higher goal.

Slide 28

The only conclusion of this study that you can make is that of course, increasing the mean arterial pressure to what we call supraphysiological levels is not efficient to increase oxygen delivery but I make some side points here, this is of course very reasonable and understandable and probably very true in what I call virgin cardiovascular patients. But some of our patients, maybe the majority of our patients are not what I call virgin cardiovascular patients. They might have some stenosis, some places in the carotid or in the renal vasculature so it might not be applicable to all patients in intensive care that we should try not to strive too high with our level and I think you should take this with a grain of salt literally that maybe some in patients higher standards might be what we’re aiming for.

Slide 29

Ok now we’ve been working until now on the fluid status of our patients but as already stated, if we want to increase the hemodynamic perfusion of the kidney because remember the first slide, this is what we’re aiming at, perfusion of our kidney, we will also have to work on the vasoconstriction of our patients especially in the septic patients. As we have already seen that fluid loading might be dangerous and once it’s inside of the patients it’s often very difficult to get it out of them especially if they’re aortic. It might be safer to go for vasopressive agents over trying to risk using volume.

Slide 30

Well, the big discussion has always been should we use norepinephrin or should we use other vasopressors? In this study published in Critical Care Medicine already 6 years ago it was clear that the survival in patients with sepsis who received norepinephrin well the outcome was far better than the patients who received other vasopressors. As nephrologists we’ve been too long too afraid to use norepinephrin because we thought that it should give vasoconstriction and that renal perfusion would go down, well this is not the case. Remember autoregulation in the kidney is completely blocked and the only thing that matters is perfusion pressure. So if your perfusion pressure goes up by using norepinephrin, this will be beneficial for your kidney.

Slide 31

The use of dopamine in acute renal failure, this has been repeated ad nauseam. This data from Kellum and co-workers shows that it is not working. Renal dose dopamine does not work and should not be advocated. Now despite that and this is very recent data 2006 you can see that a lot of people still are using dopamine in our patients. This is a sad story and we should try to remove that and we should try to go indeed to use norepinephrin as a first vasopressive agent.

Slide 32

What about vasopressin in shock? Why should we use vasopressin in shock? Well there are some reasons. First of all there is a strong splanchnic vasoconstriction induced by vasopressin. This of course will recruit more volume to the circulation instead of having it in the splanchnic circulation. The bad side of that might be that you induce splanchnic hypoxia and that by splanchnic hypoxia it might be that the sepsis is further elaborated by transmigration of endotoxins. It also gives an efferent glomerular vasoconstriction increasing perfusion pressure once again and there is data that vasopressin might be deficient in many shock patients.

Slide 33

So, it is no surprise that if you give vasopressin in patients, your systolic blood pressure goes up, you stop it, it goes down and you give it again and it goes up pointing to the fact that it’s really working. What is even more interesting is that you can see that the only thing changing is really the arterial, so the mean arterial pressure goes up because there is a systemic vascular resistance changing because of this fact but that there is no difference in heart rate, in cardiac index, in pulmonary ---, so all the other parameters remain the same.

Slide 34

Also the oxygen consumption remains the same and you can see that if you give vasopressin to these patients that indeed urine output will go up.

Slide 35

So, there might be some place to use vasopressin as a first line agent in our patients with septic shock. This has been controlled in a rabbit model where you can clearly see that if you give vasopressin to these animals, that there’s a preservation of cortical flow in septic animals where there is no preservation in normal animals that the flow in the arterial renal artery is going up in the septic animals where there is no change in normal animals.

Slide 36

The conclusion of this study was that there is preservation of renal blood flow with this vasopressin analogue during endotoxemia in rabbits and in particular to the cortex suggesting that it could be a promising agent for hemodynamic support during septic shock. Now the only -- I have there is this one. It’s particular to the cortex and as far as I remember we were always talking about acute tubular necrosis as the major problem. So it might be that by giving vasopressin that the tubule which is in the more oxygen dependent region than the kidney might not benefit that much as the cortex where the glomerulus is present and where indeed you can see that there is a higher urine output but we have no data so far on preservation of real kidney function as far as the tubule is concerned.

Slide 37

What about the use of vasopressin in hepatorenal syndrome? Well, you can see that if you start vasopressin in patients with hepatorenal syndrome that indeed there’s an increase in diuresis in these patients.

Slide 38

The only drawback of the treatment is that there is no accompanying creatinine clearance increase and that there is no difference in outcome in these patients. So this is what we can call a future treatment where it works. It gives more water out of the patient but that’s all you can expect.

Slide 39

What about Terlipressin which is an analogue of vasopressin? Where you can see that indeed if you compare it to norepinephrin that it has the same effect on the creatinine clearance, that it has the same effect on the urine flow but once again there might be some disadvantage because you see that the oxygen consumption goes down meaning that probably there is less oxygen delivery or for some reason probably vasoconstriction that it doesn’t attain the organs that will need and extract the oxygen. Of course this is at the end what we want to obtain.

Slide 40

Now, the million dollar question of fenoldopam and acute renal failure. This slide, this study refers to acute renal failure in sepsis. A study published by Morelli and co-workers, 2005. Here you can see that if you overall have the data of this study that there was no difference in serum creatinine in the placebo group versus the fenoldopam group after 5 days of administration of this drug.

Slide 41

Then there was some subanalysis of these data and you can see that in patients with a moderate renal dysfunction at the beginning of the study, so acute renal failure with a creatinine between 150 and 300 μmol/l that there might be some benefit of the fenoldopam treatment that this might not be present, if you have a higher renal function before you start but at the end there was no difference in mortality in either of the groups, so you can dispute what’s going on here.

Slide 42

We know that in another study with fenoldopam, the Stone study already published in 2003 that there was no difference neither in serum creatinine, neither in the need of dialysis, neither in survival of these patients.

Slide 43

So there is discussion which we should believe is fenoldopam working, is it not working? I think that if it is working, one of the points of differences between all these studies might be the moment that we start this therapy. I think it will be only working if we can apply it in this phase what we call the initiation phase of our acute kidney injury where there is still room that if you restore blood flow at this time, restore the oxygen delivery that some cells might not go to necrosis but might go to apoptosis which still is a more beneficial way to die than necrosis rather than if you give it at this stage where it is probably completely not helpful anymore to do anything to the restoration of your kidney function.

Slide 44

So, as Professor Mehta has already said I completely agree that if you want to intervene we have to do it fast and we need markers to show that indeed at a very early stage there is something going wrong with our kidneys.

Slide 45

The same applies a bit to the use of thyroxine which can be looked at as a vasopressive or at least as an inotropic agent where you can see that if you compare thyroxine to placebo that there are some differences in functional recovery but to the wrong extent that there is no difference in dialysis that there is no difference in days of treatment. There was a slight improvement of mortality however in this study published already 6 years ago.

Slide 46

So in conclusion these are the recommendations of the surviving sepsis campaign for patients and the use of vasopressors in these patients in ICU. You can see that vasopressor therapy should be started when an appropriate fluid challenge fails to restore an adequate arterial blood pressure.

Slide 47

Chairman: Thank you Doctor Van Biesen. Could I ask Doctor Ronco and Professor Mehta to join us here and we have a few minutes for questions from the audience. If you do have a question please come up to one of the microphones and identify yourself and ask. Just in summary what this session has provided you hopefully is an overview of this entire field. It is changing quite dramatically and we hope we have given you some food for thought. A question at microphone 1.

Quesiton: Thank you very much for your talks. About two weeks ago there was an article in the New England Journal about N-Acetyl cysteine in routine cardiac surgery with a clear advantage in mortality. Would you care to comment?

Dr Van Biesen: Well, there has been a lot to do about N-Acetyl cysteine especially in radiocontrast agents. The major problem of N-Acetyl cysteine is that it also influences the way creatinine is handled at the renal tubular site so there have been nice experiments in people where nothing happened except that they get N-Acetyl cysteine and you can see that the creatinine in these patients goes down but if you look at the clearance of cystatin C, nothing happens. So this is probably somewhat induced by some methodological errors just induced by the fact that the way the tubule handles creatinine differs in patients receiving yes or no N-Acetyl cysteine. The beneficial effect of the outcome of your kidney is to my opinion still not proven.

Chairman: If you can agree with that?

Prof Ronco: Well, yes we are going to have a metanalysis on the use also of dialysis as a preventive measure for radiocontrast nephropathy and it will appear in one of the next issues of the American Journal of Kidney Disease and we didn’t find also any difference. The interesting thing is that either dialysis or N-Acetyl cysteine seems to work very much in the hands of Doctor Marenzi which published in this New England Journal of Medicine but his data very seldom are reproduced by other studies so I think that there might be a question of selection of patients or something else.

Question: Doctor Van Biesen, in intensive care, medicine central venous saturation seems to become more used as a parameter of cardiac function and cardiac adequacy. Have you got any comments on the use of central venous oxygen saturation?

Dr Van Biesen: Well, I think the central venous oxygen saturation is a parameter that really reflects what’s going on at the organ level. The only problem there is that if it’s high, you can be on the safe side I think. If it’s low, I’m not sure what it means. If it means that the organ is working and perfused and extracting the oxygen or does it mean that you’re not able to perfuse the organs enough to give them enough oxygen. This is the question and I don’t think we have clear markers on how high or how low this oxygen tension should be then. You can measure it and I’m sure that it will be and important marker but what does it teach me? What is the clinical relevance, if it is low? What are you going to do? Are you going to try to increase it? I’m not sure on that.

Question: So you don’t use it yourself?

Dr Van Biesen: We have been using it but we do not routinely use it anymore because of that reason because the conclusions, the clinical consequences of that are not straight forward to my opinion and I think the same applies a bit to the pulmonary artery catheter. You can place it and then you get a number of data but what then? What is the consequence of that and what will it alter to your treatment and the way you assume that this patient is functioning?

Prof Ronco: Well if I can add something I think that more than one specific parameter. What we have been trying to look at is profiles. So if you can integrate different signals on different parameters in a more general picture, you might have from a combination of two or three different parameters more information than from a single one, so that’s probably a kind of you know advice I can make.

Question: Too often we get referral from CCU regarding advanced heart failure and causing acute renal failure. I don’t know what your experience is on how to manage such a case. Thank you.

Chairman: Claudio it’s for you. Managing acute kidney injury in the setting of congestive heart failure.

Prof Ronco: Well, first of all my experience is the difficulty of managing the cardiologist. The problem is again that it is very hard to define what is the pre-existing condition of renal dysfunction, what is the actual situation and what will be the situation after you treat the emergency condition because in the experience we have is that in several of these patients they might come up with a recovery from the acute phase but the dependency on dialysis after is very much present. So, I think that the management of acute renal failure in these patients should take into consideration that the high percent of these patients have to be taken care of especially when they leave the CICU and the probably the nephrologist will be the person in charge.

Dr Van Biesen: I think that my first question would be what is the underlying cause the cardiomyopathy because if you have a dilated heart it might be that by ultra filtering these patients you get them back in the Starling mechanism and their cardiac function proves, whereas if you have patients with a stiff left ventricle or with an aortic output problem or just with left ventricular hypertrophy if you reduce their preload and it might be that they completely collapse and that things even get worse. So I would be very hesitant to treat a patient with ultrafiltration or with renal support, if it’s not a congestive heart failure with a dilation of the heart as an underlying cause. I think that in other ways the outcome will be very poor anyway.

Prof Ronco: One of the things I may add is that we use a lot the blood volume measurement during extracorporeal ultrafiltration. This guides very well throughout the treatment, it tells you exactly how much the refilling is and how much is the effective volemia of these patients. So you can have a signal from this that drives your ultrafiltration and the amount of fluid you remove. We have recently also combined the use of this with bioimpedence which again in the same line we discussed before takes advantage of multiple signals that can be integrated leading to a most physiological conclusion.

Questions: Actually, my question is advanced heart failure and it’s the heart that almost failed in end stage for example and  whether you like to break this do you use peritoneal or hemo or continuous?

Dr Van Biesen: There is something to say to use peritoneal dialysis in these patients because you get a very gradable ultrafiltration to start with, you get a better preload because you have a kind of  vasopressive effect on your intra-abdominal venous structure, so you increase your preload. There is data for that. It also seems that by the convective treatment because we remove more middle molecule structures that there is some beneficial inotropic effect by the modality itself. As an alternative I think that --- or slow continuous ultrafiltration might also something that you might consider.

Chairman: I think we are at the end of our session time. I’d like to thank the speakers for being here and for all of you for staying. Thank you.