Progressively elevated BP during each SDHD from 150/83 to 205/105 range

Hello Dr. Agar,

Dori recommended I post the following.

A friend (Ben) began “in-center’ HD in March 2010 until he learned of the Home Dialysis Org and was alerter by Dori regarding the ability to conduct home hemodialysis. Ben switched to HHD in April 2010 using a NxStage PureFlow machine. He is ultra careful with diet, eating nothing with added salt, a small amount of fish, no vegetable or animal-based oils/fats, no refined sugars, all organic foods–on-balance a fairly healthy diet. He is 68 years young; 5’11” at 145 lbs.; non-diabetic (glucose consistently at approximately 85 until the last three weeks climbing to between 131 to 139—blood testing done once a week); no apparent heart condition (total cholesterol 167, LDL 102, HDL 61, Tirglycerides 52; Creatine 5.9, Bun 40, sodium ranging from 131 to 135, hemocrit 31.5 (taking Procrit shots), potasium 4.7, phosphorus 5.1, homocycseine 29.9, and 25-HYDROXY at 120 (he is supplementing with Vitamin D drops) [Note: Ben has a blood test every Monday of which the previous listed results are from 9/14/10]. Ben exercises by briskly walking approximately 1 to 2 miles several times a week.

Initially Ben attempted nocturnal dialysis (five nights on the NxStage machine), however, he was unable to sleep during sessions. Therefore, he switched to SDHD six days a week starting at 10AM for approximately 3.5 hrs/day via subclavian catheter. After each session his BP has increases dramatically–before session approximately 150/83 increasing throughout session to approximately 205/105. He has attempted to increase daily session length but his blood pressure goes even higher. The next morning, prior to starting a new dialysis session, his BP returns to the 150/83 range. He is unable to tolerate BP medications due to his chemical sensitivity having tried 10 different BP medications singly and in various combination with little to no drop in BP–all make him feel tired, nauseous and often creating anxiety attacks.

He is highly reactive to chemicals and believes he may be reacting to heparin during his dialysis sessions. His symptoms are head-flushing and hypertension.

Therefore, my questions are 1) is there an alternative anticoagulant to heparin he can use, and 2) what may be responsible for the increase in BP during Ben’ sessions?

I thank you in advance for you response,



Dear Gordon

Thank you for your question about Ben’s interesting and rather challenging problem – both for him, of course, but also for me!

You have well described his recent commencement of dialysis (March 2010), his transfer to home HD a month or so later (April 2010) – initially to overnight HD but, due to sleeplessness on overnight Rx, later to SDHD on the NxStage.

You have made it clear that (1) his diet seems excellent, (2) his salt intake is low, (3) he is neither overweight or unfit – appropriately attending to both - while (4) his dialysis biochemistry seems broadly excellent (though I will note one or two instances where that seems not to be so later on), (5) he does not have diabetes (6) indeed he appears, broadly, to be a shining example of the ‘good dialysis patient’ with – albeit viewed from >12,000 miles distance and with only the data you give to go on – pretty good ‘dialysis numbers’ too … yet, he clearly appears to have surprising accelerated dialysis-related hypertension.

Hmm … where to start?

The first thing to say is that although the overwhelming proportion of hypertension in dialysis patients is due to pporly controlled fluid intake, salt excess, under dialysis … the things I have spent pages on at this site explaining … Ben’s problem doesn’t sound quite like that.

To begin … there are a few gaps – indeed, more than a few – in my knowledge of Ben.

One thing you did not give in your summary … and it may be highly pertinent here … is the cause of his kidney failure! It isn’t diabetes but … he is male and in his mid-late 60’s … and he has a high homocysteine level – at least I think it is high. It would be in the units we use here! You also didn’t state if he has been or is still a smoker.

One of the problems I wrestle with on these pages, Gordon, is that US biochemical measures are quite foreign to me … we use, along with all other countries, the SI unit system. The US remains on the older mg/dL system. But, as best I could, I checked the units you gave and all would suggest ‘good’ numbers … barring the homocysteine level.

His maleness, his age, his high homocysteine level (a pro-accelerant for vascular disease) … all are potential ‘hints’ to the possibility Ben may have underlying vascular disease.

Oh … and before I start … one thing I do not think this is likely to be is a reaction to heparin. Let’s get that out of the road to start with.

One of the potential causes of hypertension – exacerbated during or by dialysis – might be renovascular hypertension.

If he has a renal artery stenosis – either recognized and known or, more likely, unrecognized and unknown … maybe till now … with this hypertensive response to dialysis being the ‘un-masker’.

I would note, that his pre-dialysis BP’s are high too … and while he is ‘unable to tolerate BP medications, having tried 10 different medications singly and in various combinations with little or no drop in BP’, this suggests at no time is his BP controlled.

Interestingly, the very fact that he has had such a struggle with his BP control and is now on dialysis makes me suspicious of either underlying renovascular disease or, less likely but still potentially, a phaeochromocytoma.

Has these been sought? Have either or both been excluded?

Did he has renal angiography (formal or CT-related) as part of the investigation of the cause of his declining renal function prior to beginning dialysis?

Acute volume reduction … as is an integral part of the dialysis process in most patients as ‘dry weight’ is sought … can activate the renin-angiotensin system and/or the sympathetic nervous system.

The effects of that activation – primarily renin release and a subsequent induction, through angiotensin, of acute vasoconstriction leading, in turn, to acute hypertension can provoke in some dialysis patients a phenomenon that has sometimes been described as paradoxical hypertension. Is this rare? … yes, relatively. Is it rea? … also yes.

In this situation, the usual hypotensive response to volume depletion is overcome with the vasoconstriction resulting from angiotensin activation triumphing over the more usual hypotensive outcomes we see in most dialysis patients as a result of volume reduction. As the same applies to activation of the sympathetic nervous system, the outcome of ‘twin’ (or dual) angiotensin and sympathetic nervous system stimulation is what is known as paradoxical hypertension … induced by dialysis.

While this is an uncommon response of the BP during dialysis, it is nevertheless a well-documented one. The KDOQI guidelines contains a small subsection on this phenomenon which reads …

Paradoxical rise of blood pressure during dialysis (JA editd)

Hypertension induced by HD is a topic that has received little attention. It occurs in a small number of patients during HD. The causes of this phenomenon have not been well worked out. Sometimes it is precipitated by removal of certain antihypertensive drugs during dialysis.

Hemodialysis reduces blood levels of some ACE inhibitors (enalapril, ramipril) but not others (benazepril, fosinopril, methyldopa, atenolol, acebutolol, nadolol, minoxidil and nitroprusside); by contrast, levels of clonidine, carvedilol, labetalol, CCBs and ARBs do not change significantly.

At times, excessive volume depletion may result in hypertension rather than in hypotension. This has been attributed to excessive stimulation of the renin-angiotensin system precipitated by the decrease in blood volume.

An alternative possibility, which has not been properly investigated, is that this might be the result of excessive activation of the sympathetic nervous system and resulting vasoconstriction.

The explanation of this phenomenon remains elusive

See …

How might this apply to Ben and what I have said, so far?

Well, let’s just assume for a moment that my wild assumptions do turn out to be so and that he does have renovascular disease and covert renal artery stenosis.

As dialysis removes volume, the usual response is hypotension but we are assuming Ben’s ‘milieu’ is one of an activated vasoactive state in which the RAAS and sympathetic nervous system response is a vasoconstrictive one. Incidentally, the symptoms of this state are headache, flushing and accelerated hypertension.

Dialysis begins …

The fall in volume stimulates renin production from his still-capable-of-responding kidney(s). Angiotensin is activate. Acute vasoconstriction occurs. The blood pressure rises. This rise overcomes the more usual BP-lowering effects of dialysis-related volume contraction and paradoxical hypertension with anxiety, flushing and headache and ‘I feel lousy’ symptoms resulting.

Could this be related to anything else? … yes … has he had a phaeochromocytoma excluded by either biochemical marker assessment or imaging of his adrenals?

One off-the-wall thought is … and there are well-documented reports of just this very outcome … if there did is a tight renal artery stenosis - and especially if it were bilateral - and this/these could be dilated/stented, then there is a possibility and there are case reports - although rare - where patients have been able to come off dialysis after the restoration of renal blood flow. I am not suggesting that is a likely scenario for Ben … but it is always worth thinking about.

Gordon … something odd is afoot here. While a further effort to introduce BP pills might be a good idea … my guess is something like labetalol in the 1st instance … that’s not, to my thinking, yet the whole answer here.

I’d be chasing, and chasing some more, at this point to exclude a hormonally active cause for his hypertension: RAS and/or a phaeochromocytoma being at the top of my list. I don’t think I’d just sit by and scratch my head.

The response is too intriguing and the potentials too strong to ignore.

All this needs to be discussed with Ben’s managing team. I may be way off beam. Nevertheless, the issue of paradoxical hypertension is sufficiently well recognised to follow up a step or two further with some smart thinking.

Dear Dr. Agar,

Thank you for your most rapid, extensive and informative reply. I apologize for not including more information in my original post, however, I will attempt to provide additional information upon consulting with Ben later today --I am in Southern California; Ben is in New York.

At the moment I am able to address some questions and information you requested. So, just to get a “jump” on things, here goes. Be forewarned, I am a nutritionist thus quite out of my area of expertise when it comes to nephrology, nevertheless, I will give it a go.

Ben is a non-smoker and to my knowledge has never smoked (I will confirm). He was tested for renal artery stenosis resulting in a negative diagnosis. As for pheochromocytoma–I had to look this one up :slight_smile: – I will check with Ben. I do not believe he had a renal angiography since he would not want dye injected, however, I will ask (possibly the following paragraph regarding a renal sonogram will answer your question).

A sonogram Doppler ultrasound study was conducted in 8/2009. The doctor’s report stated—‘The right kidney is 9 cm with no hydronephrosis and 3 cm simple cyst upper pole and 4 cm simple cyst lower pole (no change is size since last examination). The right kidney is 9 cm with no hydronephrosis. Renal Doppler shows normal blood flow in the right and left renal arteries, aorta and arcuate vessels bilaterally.’ At the end of the report the following observations: ‘Intervesical prostate volume increased 4 cc; 5 mm right prostate lesion; unchanged renal simple cysts; normal vascular abdominal and renal parenchyma, and unchanged bladder hyprotrophy.’ The report also covered observations regarding the prostate, which, upon you request, I can make available.

Ben was hypertensive prior to beginning HD with BP ranging around 190/95 most of the time (I believed the BP has been a challenge for several years). A few BP meds would take his BP down to about 160/85, however, as I stated in my original post, he was unable to tolerate them.

Ben was diagnosed in 2005 with CKD. The exact cause has not been determined–could it be caused by immune reaction–IgAN? He chose not to have a kidney biopsy. However, he believes his CKD may have been caused by an enlarged prostate dramatically restricting urine flow causing possible hydronephrosis resulting form Ben self-catheterizing on many occasions rather than going to the hospital. Subsequently Ben had what is called green laser treatment to reduce the size of his prostate.

Over the last six years Ben attempted to improve his CKD via alternative medical approaches --herbs, close to a vegan diet, reduction in exposure to allergic foods, acupuncture, elimination of environmental EMF, almost total elimination of exposure to chemicals (he has sever multiple chemical sensitivities resulting in purchasing a house in the woods, almost tearing it to the ground and rebuilding with all non off-gassing materials, even going to the extent of grounding his house from EMF…and by the way, the reason I am interfacing for Ben via this medium is because he does not use a computer due to his EMF sensitivity.

In an attempt to cure or at lease stop his renal function decline, Ben sought out the best experts (and some not so expert) from around the world in both allopathic and alternative medicine. On numerous occasions he has going so far as to fly-in experts from around the world to his home for consulting, and personally traveling to foreign lands for any promising treatment. He has stopped at nothing in an attempt to slow, halt or reverse his kidney deterioration.

Prior to beginning dialysis Ben presented with ESRF with an approximate 11% kidney filtration rate. His kidney function began improving after beginning an almost vegan diet in late October 2009, including eliminating foods to which he tested allergic–foods which possibly caused allergic edema. After ten days on the new diet his creatinine levers began dropping from 5.9 to 4.3 over several months with filtration rate increasing to 15.1%; however, the numbers began reversing in Feb/March causing him to finally bite the bullet and begin dialysis. Due to this increase, plus high BP and other blood markers continually fluctuating out of range, especially the following: sodium[L], potassium[H] and hemoglobin[L]—just to mention a few, and Ben being rushed to the emergency room of several occasions to bring him back into homeostasis. Due to these emergency situations and other compounding factors previously mentioned, it was highly recommended Ben begin hemodialysis earlier this year—very reluctantly he did (note: he has a kidney donor on standby, however, due to the fact that if he does receive a transplant he must begin taking many meds—which most likely will dramatically reduce his quality of life—he is not moving forward with a transplant).

You wrote: “An alternative possibility, which has not been properly investigated, is that this might be the result of excessive activation of the sympathetic nervous system and resulting vasoconstriction.” Interesting! This touches on something I found in my research while attempting to learn what might be causing Ben’s increased HTN during dialysis. Are your aware of the effect of dialysate temperature on patient hypotension and hypertension? In two interesting studies (links provided below) a small change in dialysate temperature dramatically increased or decreased BP, i.e., warmer temp increased hypotension; cooler temp decreased hypotension, therefore, I extrapolated that cooler temp will increase hypertension and warmer temp will decrease hypertension. The study stated that a dialysate temp of 98.6 degrees F stabilized BP in hypotensive individuals. Ben’s dialysate has been in the cooler range. He is about to run an experiment by increasing the dialysate temp to between 98.6 and 100 degrees F. to see if it reduces his hypertension [the 1984 study link is at ] Another study regarding the same issue conducted in 2006 is at

A second area of interest and possible assistance in lowering Ben’s BP is the amount of Na+ contained in the dialysate used. Ben is presently using a dialysate with a concentration of sodium of 140 mmol/L; however, Ben’s serum sodium is 131 mmol/L. Several studies [2004 and another] show that reducing the sodium concentration of the dialysate to the patients sodium serum level lowers BP and also interdialytic weight gain. Therefore, Ben received permission from his nephrologist to seek out a source to customize a sodium-reduce dialysate solution use. We are attempting to locate a source but finding it most difficult. [The 2004 study link is at and a second is study overview is at

Well, that’s about the best I can do for now until I speak with Ben later today.

As you have read, Ben is extremely motivated to improve his health. To that end he is willing to consult with anyone appearing to have information leading to a possible solution(s) to his challenges.

And thank you for your kind attention to Ben’s situation. If you are open to continuing this post-discussion we are in advance most grateful.

Warmest regards,

Gordon for Ben

PS. Please excuse any errors in this long response–it is now 3:45 am and as I quickly review what I have written my brain may not quite cooperate in catching errors.

The intent of this site, first and foremost, is to try give overview information to patients regarding the mechanisms of and issues to do with haemodialysis – information that might be of broad interest to haemodialysis patients. It is not the intent of the site to enter into - nor will I wittingly participate in – deep discussions with individuals … and in this case, with a third party … regarding very personal (and in this case, quite unique and highly unusual) medical problems.

While I agree that there is clearly a fine line distinction here – and I may at times unwittingly cross it unintentionally where the distinction between general interest discussion and individual advice can blur, I have tried, where possible, to give answers that cover topics that may interest the majority rather than delve into specifics for any one individual.

Your original question to me was one which seemed, at first look, to be one of general interest: the problem of a progressively rising blood pressure during dialysis. This is an issue which can be a significant problem for some (albeit a small sub-group) of dialysis patients – albeit that the reverse is more commonly seen in the majority, where the blood pressure falls, sometimes rapidly, during dialysis due to acute volume contraction.

As rising blood pressures and, as I noted in my last post, this is sometimes described as ‘paradoxical’ hypertension, can indicate the dialysis-related activation of various vasoactive pathways - like renin and the sympathetic nervous system – I felt my answer should cover, albeit superficially, some of those possibilities.

I now find the discussion has very much drifted into the specific issues of a specific patient – and, in addition, issues which are far from the purview of most dialysis patients.

As such, I find I am being asked to comment on or to in-build into my thinking on these questions some rather esoteric issues … such as electromagnetic field (EMF) hypersensitivity. This, in particular, is an issue (1) of which I have no personal knowledge (2) in which I have no expertise (3) of which I am deeply uncertain that it hold validity and (4) that I find hard to relate to the dialysis issues that confront your friend.

As for the effects of temperature on blood pressure and circulatory stability – yes, there is long-standing data on this. The observations you make are, broadly, in line with that data though I would doubt that the degree of dialysis-related hypertension that you relate is occurring would be blunted by changing the temperature of the dialysate alone.

As for altering the sodium concentration of the dialysate – this is a well described and known dialysis practice called sodium modeling that has been around for a long time and which, while particularly popular through the 1990’s, has largely disappeared from common practice in most dialysis centres. It is used, however, now and again – indeed we still occasionally invoke the practice in selected cases – and it may well be worth consideration. However, this should only be in consultation with, under the guidance of and with direct control through his managing dialysis team. I would not presume here, at this site, to advise further regarding this other than to say it is potentially a useful exercise. It is worth noting, however, that the serum sodium levels you quote that he maintains might suggest that – just like with dialysate temperature manipulation – he may not get a huge benefit in terms of blood pressure control through manipulation of his dialysate sodium either.

I have to say that, personally, I would be attempting to achieve improved blood pressure control through medication. While I understand he has had difficulties with various medications, I would suggest that he is at significant risk from the blood pressures you have mentioned and that his risk from untreated surges of his blood pressure – especially on dialysis – exceeds any real or anticipated potential risks that might accrue from antihypertensive medication.

Gordon … these problems are not ones that I feel confident to comment on further at this site. They are clearly far from the norm and would appear to require hands-on, on-the-spot, expert management. It would be unwise, in the extreme, to attempt to do this through an internet discussion site such as this.

I would encourage his engagement with his managing team to work through all these problems. They are not ones that can be dealt with, either from half a continent away in California or a continent and ocean away in Australia.

I am sorry I have not been able to assist more – but I do not think that the internet is the vehicle for conquering this difficult set of problems.

Dear Dr. Agar,

Thank you for your thoughts and inputs regarding Ben’s most challenging situation. I agree the Internet is not the medium in which to delve into numerous specifics regarding Ben’s situation. Your time and expertise is undoubtedly best suited, as you wrote, for broad segment of hemodialysis patients, thus, we respect your request.

l will share with Ben the valuable insights and information you presented so he can provide such with his dialysis team.

Warmest regards,

Gordon for Ben


Just a quick question … how is Ben doing? Is he OK? I have just been wondering if some/all of his problems got a bit sorted?