Hello, I am 42 yo, African American Male that's been dealing with High Blood Pressure for the last 3 years, since I've turned 39 it seems, Drs have me on multiable Meds and nothing seems to work to bring it down, in the last year, My creatine has gone up to over 9, and Drs tell me I need Dialysis, So Ive been going to dialysis and when I get on the machine my Blood Pressure goes sky high 210/115, within the first hour and never comes back down till the next day 106/88 (My normal), the techs at dialysis don't seem bothered by this at all, while I feel that Dialysis is hurting me , not helping me.
I still Urinate, 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, dehydrated. I feel as if I'm being over dialyzed, 3 days a week @ 4 hours each is way too much for me, no one else in the clinic seems to have this issue, they all get off the machine and their blood pressure(s) are normal or low, but Mine gets up really high 205/108, I'm very concerned that dialysis is doing more harm then it is helping me, but they don't listen to me and continue to do things same way every time, I've been going though this for over a year and 6 months now.
What Should I Do? Please Help.
Dear Wayne ...
I hope you don't think I am ignoring you question - I will answer it early this coming week ... i am rather flat out this weekend, so I hope you can be patient another day or two
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 (an) 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:
1. 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.
2. 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
Last edited by John Agar; April 16, 2012 at 02:11 AM.
Dr. Agar wrote to Dr. Chazot, and here is what he said:
"Dear Wayne, Dori and John
Thank you John for inviting me to this forum. I quite understand Wayne’s concerns regarding the rise of is blood pressure (BP) during the dialysis session and he is right. This has to be fixed because it increases risks for future complications such as pulmonary edema, heart failure or stroke.
John has extensively addressed the problem, kindly referring to our review, especially the cardiac mechanisms of the BP increase. I share totally his opinion that fluid (sodium+water) accumulation is the cause of blood pressure increase during the session and that Wayne never reached the dry weight. The important study by Chou (Kidney international 2006) has ruled out the responsibility of antihypertensive agents removal during the session, and the role of the renin and sympathetic nervous systems. It seems that something happens to the vessels’ endothelium. The endothelium is the inner thin layer of cells of the vessel wall. It is very active to command the flexibility of them with the synthesis of agents like nitric oxide which dilates (opens) the vessels and endothelin that constricts (narrows) them. When narrowed the pressure inside increases. It is possible that plasma refilling during the session (that is the shift of sodium and water from the tissues into the vessels ) triggers these changes in the endothelium increasing the blood pressure.
In my opinion, several informations are needed to cover the understanding with some comments:
- Dialysis time (how many hours per session?) and dialysis frequency (How many session per week?), the prescribed blood flow (speed of the pump), the filter area and the predialysis urea level (urea concentration in the blood before dialysis): insufficient dialysis with high urea level may be an explanation for the cramps.
- Prescribed sodium concentration of the dialysate: Frequently sodium is concentration is raised to a high level (>140 mmoles/l. We usually stick at 138 mmoles/l in our unit) to avoid BP drops and cramps. There is no data showing the relationship between a high sodium content in the dialysate and the rise of BP during the session as far as I know. However a high content may participate to thirst and fluid overload, especially if the sodium concentration before dialysis in the blood is low. If the prescribed sodium in dialysate is too low (lower than in the blood) it may trigger cramps. However I doubt it is the case for Wayne.
- Moreover, has Wayne been prescribed a restricted sodium diet? This is very important to avoid sodium load. Again and again flee away the processed food companies…
- I am not aware of the availability of the BCM device in the US. This tool would give information on the amount of fluid Wayne has accumulated (There are however discrepancies in patients with high body mass index – the ratio between the weight and the height x height).
- I am surprised that BP is so low during the interdialytic interval. Ambulatory monitoring would bring important information and I bet BP is not so low in average during the interdialytic interval.
- Last but not least, peeing does not mean Wayne is not fluid overloaded for sure. Searching for dry weight by decreasing the weight at the end of the sessions by 200-300g per session will correct the rise of BP during the session as John wrote. Probing for dry weight may decrease the amount of urine. However one has to choose its camp: fluid overload and preserved urine output versus dry weight with the risk of reduced diuresis. This is a great debate….
- Overdialysis never exists. Never forget we provide our patients with standard dialysis treatment no more than 15-20% of normal renal function….
I hope this will help Wayne.
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