This is such a complex question … and one, I am afraid, that also has a very difficult and challenging answer.
Your question goes directly to a well known, but poorly understood and even more poorly treated problem common to around 10-15% of all dialysis patients.
It is called intra-dialytic hypertension. It is a serious problem and you are right to be concerned about it and to be seeking ways to minimize or manage it. It must not be ignored. It matters – a lot – and it carries a worse prognosis if it is allowed to continue unresolved. It has long been a phenomenon of interest – especially to Bernard Charra and, more recently, to Charles Chazot (both from the renown Tassin group in France) - whose track record in this area is second to none. Charles and his co-worker Guillaume Jean(whom unfortunately I do not know) have written a very nice summary of the problem:
Intradialytic Hypertension: It Is Time to Act. Charles Chazot, Guillaume Jean. Nephron Clin Pract 2010; 115: c182-c188
… though it is, of course, a medical paper and is therefore full of medical words and complexities - though I will try to demystify it here for you.
If you want to try reading it, you can find Charles’ paper in full at …
… and if you do nothing else, print it our in pdf format and take it to your nephrology team.
One thing is important above all else: Intradialytic hypertension must not be ignored or swept under the carpet. There are answers. There are steps to take. Again … if nothing else, draw Charles paper (as above) to the attention of your treating team then work through the steps with them till your BP issues are solved – as they can be!
The abstract to Charles’ paper reads as follows … with my additions in ( ).
Intradialytic hypertension (IDH) is defined by blood pressure (BP) values during and at the end of the dialysis session exceeding BP values at dialysis onset. It occurs in around 10% (some series put it higher: JA) of hemodialysis (HD) patients. It is associated with HD patients’ (higher: JA) hospitalization (rates: JA) and I[/I] increased risk of death. Many hypotheses have been proposed to explain this phenomenon. Recent studies and reports highlight the important role of fluid overload, hemodynamic changes, and increased endothelin levels (endothelin is a hormone that causes blood vessels to constrict and which thus increases the resistance of blood vessels to blood flow and makes the heart have to pump harder and generate a higher pressure to permit blood flow: JA). The importance of other hypotheses such as the renin-angiotensin system activation (I will explain this in this answer later: JA), sympathetic overactivity (this too: JA) and ionic variations seems secondary but it deserves to be confirmed. Fluid removal remains the key point for treating IDH. (= my use of bold type: JA) Several important unanswered questions remain and the need for further research is highlighted.
NB: I hope my ‘interjections in italics’ weren’t too annoying for you.
Though there is much complexity to the topic – as shown if you but take a glance at Charles Chazot’s paper – it really does seem to all come down to volume overload and sodium excess.
The commonest response to that is: but I don’t gain much weight, I don’t retain fluid and I cramp on dialysis and feel I am being dehydrated! You said as much yourself – and so, too do others like you. Yet, odd that it may seem to you, you are actually sodium overloaded. I know you will find it hard to accept that – but it is by far the most likely reason that you are as you are.
Anti-hypertensive medications (BP pills) are not the answer.
One thing you didn’t tell me, Wayne, was your overall body weight. I don’t know if you are a big guy, but if you are, your comment that … … “I never gain more than 0.4kg / 0.6kg of weight, I don’t retain fluid, I always get cramps within 2 to 3 hours of being on the machine … and I’m very concerned that dialysis is doing more harm then it is helping me” … … may be because sodium and fluid can ‘hide’ so well that they may not be initially apparent.
You may think your dry weight has been achieved – but, sadly, it never, ever has been. Not once. You are kilos over it. It’s just that your circulatory ‘triggers’ have been reset way too high and need to be reset again, but down at a normal BP … and while this is a slow and tedious thing to do, it is an enormously rewarding exercise.
The key graph to understand is the Starlings Law graph – it is well explained in the paper. This first of all ‘laws’ of cardiovascular medicine shows how it is that as fluid is removed, the BP rises (initially) and the panic stations default then is ‘take him off, take him off’. You have to be brought down the initial up-slope on the left of the curve – but sadly, you ain’t making over the top from right to left. And you are right to be anxious that “dialysis is doing more harm then it is helping me “ … for until you crest the curve and embark down the left hand side to normality, it is doing just that.
You must be ‘de-sodium’d’. Your BP control will follow. It really will. Your BP meds need tapering as your weight is being reduced. My bet is that if your weight is reduced by sodium (and fluid) removal, gradually, you will find that you actually won’t need BP meds at all.
Your team can try using a BCM (a Body Composition Monitor: these are made by the Fresenius Medical Care company) to help map the course but, more importantly than that, you will need longer, slower dialysis treatments to slowly work your weight down as your BP pills are reduced.
Please, ask your team to read the Tassin work. While they are not the only experts in this space, they are (and have been) the benchmark in ‘good dialysis’ the world over, for as long as I care to think. Work with your team – and you will need patience as it may take 4-6 weeks to achieve BP-normalised and BP-pill-free dialysis – and you will overcome this.
In addition to sodium excess = the real ‘baddie’ here - there are other likely secondary factors at play:
the Renin-Angiotensin-Aldosterone System (RAAS) - which is a hormonal system designed to sustain the blood pressure but which, if over-activated, leads to hypertension. ACE inhibitors and ARB receptor blockers (the ‘prils’ and ‘sartans’) counteract overactivity of the RAAS. It is thought that as volume is removed on dialysis, the RAAS can be switched on in response to ‘hypovolaemia’ (low blood volume) and ‘paradoxically’ force the BP up during volume reduction on dialysis. Hmmmm … while there is some evidence that this can occur in select cases, its not too convincing and the RAAS is thought to only play a partner role to chronic sodium overload, at best.
the Sympathetic Nervous System is a parallel neuronal (nerve) system in our bodies that, like the RAAS, helps to constrict smaller blood vessels and raise blood pressure by increasing the resistance of blood vessels to flow. If blood vessels are ‘constricted’’ the heart pumps against a higher pressure in the circulation and this pushes up the blood pressure. While also a potential mechanism for IDH, again, like the RAAS, the Sympathetic Nervous System is thought to play but a secondary role.
Now - after all that - I am aware I have not explained this all as well as I might.
I wonder if Dori Schatell might ask Charles Chazot – whom I think she knows well, as do I – to ‘guest comment’ on this post. I am sure Charles would make a better fist of explaining this unique and very complex issue in lay-terms.
I will draw this to Dori’s attention and will hope that Charles takes up the offer and the challenge