Hi Dr Agar,
I would like to know if and why in-center hemo deteriorates remaining renal function. Before you go on dialysis you are already in decline, wouldn’t failure in general be the culprit. Does in-center maintain function? Does home hemo maintain function? Thanks for your help. Dan
Now, Dan, that is an awesome question … and the answer opens an enormous (but very important) and largely unknown area. I will try to explain … and, sorry, its a loooong explanation! …
As your own kidney function dwindles – from time and progressing disease – your doctor will make a decision that it is time to ‘ready’ you for dialysis
at eGFR 25-20 … pre-dialysis education sessions for you and your family about the ‘choices’ (whether HD or PD, home or facility) and about the ‘hows’ (the way dialysis works, what you can expect, what might go wrong, how it can be addressed and issues around discontinuation if all is bleak and, if so, who might make those decisions for you if you can’t yourself)
at eGFR 20 … an native AVF if HD is the choice
an ESA to treat the anemia … the main driver of the symptoms which accompany failing kidneys
Then … at an eGFR of somewhere between 8 and 10 (I use 10 as my guide ) though the exact moment will be determined, too, by how you feel, how your heart is, what other ‘co-morbidities’ (other medical problems) might co-exist – a decision will be made to start you, all readied up and in-the-know, on your modality.
That means at start of dialysis, you will have ‘x’% of your native renal function left (and though I want to make it quite clear that eGFR does not equate to %, as a normal eGFR is +/- 100, eGFR can be thought of, in a broad sense, as similar to a % figure). That is the remaining function that doctors call ‘residual renal function’ ( I am going to abbreviate it from here on and call it RRF)… and it will continue to dwindle after you start on dialysis, if other factors don’t affect it, at about the same rate it was dwindling away before you started dialysis.
That RRF is really an important component. It usually means – if nothing else – a residual urine output! And, though there mightn’t be too much waste being cleared, a residual urine output means that fluid is! And that means a freer intake of fluid on dialysis. I mean … if you are peeing 1500ml a day, even if it’s got damn all, or way too little, solute (waste) in it, that means you can drink more freely as you are not depending on dialysis alone for ‘volume’ control. There will, of course, be some added solute clearance too – to your benefit – but it’s the comfort that RRF affords fluid intake that is the most appreciated by the patient.
PD traditionally preserves RRF – especially over the 1st 18-24 months of dialysis. This has been well shown. The PD patient tends to still pee! That allows easier fluid management and free® fluid intakes.
HD … traditionally abolishes RRF quickly after dialysis start – though there is some suggestion (and I believe this to be a real phenomenon) that frequent and long dialysis preserves RRF (like PD does) while, on the other hand, short hour and conventional 3 x week x 3-4hr treatments do not …
OK … why?
Each time a patient starts on a haemodialysis treatment, there will be an ‘amount’ of fluid to ‘take off’ … an ultrafiltration rate (UFR) will be set and, typically, this can be 700-800ml/hr (or more … sometimes lots more). This fluid is removed from the circulation. BUT, the body can’t replace that fluid from its’ stores (the extracellular and intracellular compartments) … and for an explanation of this, can I draw your attention to my Webinar at the HDC home page on ‘Fluids’ … at more than about 400ml/hr. So, any UFR greater than 400 will be removing (roughly) that UFR – 400ml from the circulation each hour of dialysis.
Let’s say that the set UFR is 950. Then 950-400 = 550ml (>½L) is being removed from the circulation each hour or dialysis.
Not only does that destabilize the BP, cause symptoms on dialysis and drop the BP and cause ‘flats’ etc … BUT, and here’s the (very long) answer to your question … it drops the perfusion pressure to your remaining renal tissue – your own native, struggling, but still partially functioning kidneys!!!
So, each dialysis induces renal ‘ischaemia’ … that is, a reduction in blood flow to the native kidneys. The greater the UFR exceeds the plasma refill rate capacity of the body to restore blood volume (about 400ml/hr), the greater the effect the dialysis will have on the circulation and the greater the reduction in blood flow (and oxygenation etc) to the native kidneys that will occur during dialysis … see the Webinar again.
It’s like subjecting the native kidneys (struggling already as they are) to recurrent episodes of acute renal ischaemia … or recurrent acute kidney injury from tissue oxygen deprivation.
Add this recurrent insult to the natural decline in RRF from the underlying disease process, and RRF just goes out the window, urine output falls, fluid restrictions worsen … and if the patient cannot comply with those, the greater the fluid (read weight) gain between dialysis treatments and the greater the next UFR … and the more severe the next dialysis-treatment-induced ‘dose’ of native kidney tissue hypoxia (under-perfusion and low oxygen supply) will be!
PD, by contrast, is a gentle, 24hr a day treatment with much less minute-to-minute effect on the circulating blood volume. It doesn’t drop the blood volume at all. Thus, native kidney ‘perfusion’ is unaffected. So, though the underlying disease may still eat away at RRF, a dialysis-cause circulatory change will not.
NHHD (especially if long and frequent), has a nice low UFR … a UFR well below the rate at which the body can no longer keep pace by refilling the plasma volume from its stores. So, like PD, NHHD does not disturb the circulatory blood volume. By deduction, therefore, one might expect NHHD to similarly preserve RRF, as PD is known to do. Do we know this yet? No … though some are working to prove (or disprove) this theory.
Short daily is, in this respect, no different to conventional dialysis. As time is halved (4-4.5 hrs down, typically, to 2-2.5 hrs) and even though frequency is doubled (3/week to 5-6/week), the UFR remains high. As such, short daily has the same effect on the plasma volume as conventional dialysis regimes.
Dan … that was a long answer … but the question was a ripper and deserved it.
John Agar
Hi Dr. Agar,
Nurses would always tell me I was a model patient as I would always come in with a very low fluid gain. But I would tell them that I had no choice in the matter as I could not gain more or I would pay the price with cramping or crashing on tx. After about 2 years, I moved out of state and was in a new unit. I was feeling more positive about dialysis as the new unit was a lot nicer. At one point, I decided to challenge my dry weight to see how much fluid I could comfortably gain and without becoming hypotensive. I found that I could go to 3.0 and with one drink on the tx, plus prime and rinseback that brought my goal to 3.5. Every tx went smoothly and I even felt well post tx. for about 6 months.
In this unit we had assigned chairs so I had the same machine each tx. Then, one day, the biotech took my machine for a maintenance update. I had been observant of all the #s on the machine and the only thing that changed was the conductivity. The conductivity on this FR H machine had always been at around 14.0 - 14.5. When the machine came back from the update, the conductivity was now reading 13.4 - 13.9. That very first tx back, I became hypotensive at my usual goal. I took the goal down more each tx, but had one symptomatic tx after another. We tried using another machine, but still had problems. I noticed that the other machine had low conductivity too. It was only when I was put on a machine that had higher conductivity that the events stopped and I could return to the 3.5 goal again.
Next, I moved out of state again and into another unit. From the first day in the new unit, I could never again reach a goal of 3.5. In this unit, the sodium modeling was set differently then my previous neph had ordered it. And I was switched from machine to machine with different conductivity rates. I had to drink less in order to keep my goal down so as to not have an event. Then, in time, I noticed I could not comfortably drink as much as I had previously and my output was more diminished.
The next move was to short 6x txs. From the very first week, I noticed that my output went down to almost nothing. I asked other SDD patients if they had a severe drop in output when they went to short 6x and they said it had happened to them too. Now on nocturnal txs, it is the same. My average goal is about 1.0 and the highest goal I have following the day off is around 1.7 at the most. I thought long nocturnal txs might allow me to pull off more fluid on txs without hypotensive events, but I can not go past about 2.0 without problems. Actually, I should say that I found that I could remove more fluid on nocturnal txs then with SDD, but I wound up cutting back as my blood pressure was looking too low. I did not have symptoms during the day, but the pressures looked too low, so I increased my dry weight, thus removing the same goals as with SDD…
Despite being on nocturnal now, it does not matter, because my drinking capacity is very diminished. I drink very little throughout the day as I have little thirst, and if I do try to drink just for the sake of drinking more, it feels uncomfortable. I tend to feel a little thirsty in the afternoon, but the only thing I seem to want for my thirst then is fruit containing fluid like melon. So, most of the drinking I do is at my last meal of the day. Then I drink more normally and often have a small bowl of soup. This fills me up for the day and I am feeling too full, but I don’t hold the fluid long as in a short time, I begin my nocturnal tx. And withing about 1-2 hrs, I feel well again as the fluid is removed and my system settles down.
I have gone through a lot of changes in my drinking capacity and fluid goals and I always wondered how much was attributable to the various scrips I was on as well as machine variables like conductivity and sodium modeling. And I wondered how much the different scrips etc affected urine output Also, one time I had the opportunity to be critlined and with the Critline machine ( are your familiar with Critline technology?), I was able to take off .9 more than I could with my txs at that time ( this was in the unit where I could not longer set a goal of 3.5). Interestingly, I always remember it as the best tx I ever had on dialysis as I could breathe in and out freely in a way that I had not been able to do in years and had a very good appetite directly following tx., which I never had, and wanted to go out for a good supper. Of course, as soon as I had supper, I felt too full again : (
I later got to know a nurse at Critline and she explained to me that no matter what a person’s size, the circulatory system can only hold and safely remove about 2.0 per tx. without affecting the heart etc. So, Dr. Agar, if you can make any sense out of my progression with fluid removal, I’d love to have your thoughts when you are back from leave.
A short answer to your dialysis journey, Jane, might be this … but, first, please re-read my initial answer to Dan as the answers to most of your issues are contained within that 1st answer.
You started dialysis with, probably, a residual renal function (RRF) equivalent to an eGFR of maybe 8-10 ml/min. Let’s assume that.
Things remained stable on the fluid front for you for quite a long time, maybe longer than many/most other HD patients are as lucky to have enjoyed as you were.
You had a urine output, sustained by your RRF, which, though it was dwindling slowly from your base disease (largely unbeknownst to you), was still giving you some leeway with your fluids through those 1st two years.
Then … zam! … your machine changed and the sodium profile was reduced from 140-145 to 134-139 in your new machine.
The sodium concentration of the dialysate is used to ‘drive’ or, to use a word you tend to like (but I tend not to), to ‘script’ the movement of water.
A sodium level (concentration) in the dialysate that is ‘set’ to a lower concentration (say, 134-139) than that of your blood concentration (which is more like 140-145) will drag water from your circulation, across the membrane into the effluent and away. A sodium level of 140-145 tends to be in more balance with your blood.
NB: There was a time when there was a fashion (one I do not personally like) of ‘sodium ramping’ … but let’s not go there – it’s NOT easy ground and it’s not, in my view, a good practice to adopt except (maybe) in rather rare and special circumstances that are NOT useful to explore in these pages. I know some might disagree with me on this – and that’s fine – but I am sticking to my view!
When you were changed to a machine set to a lower sodium, water was sucked from you, your BP dropped, you cramped, you became hypotensive and symptomatic … and, after re-reading my 1st explanation to Dan (see above) you will now realise that your native kidneys experienced (as you were) a reduction in perfusing blood volume … your kidneys were being made ischaemic (lowered perfusion, blood flow, and oxygen delivery) as a result.
So, down went your RRF! … and once gone, it won’t return.
Your volume was ‘re-set’ lower but, in the re-setting, you lost your RRF and the flexibility of a urine output and of fluid intake freedom that allows (again, see my 1st answer in this thread).
This is the way with most haemodialysis patients … and most don’t have the luxuries of urine output and fluid freedom that you seem to have enjoyed in those early months … so, in a way, you can count yourself blessed that your RRF ‘kicked’ for as long as it did.
As I also made the point in my 1st response to this thread that short daily does exactly this, too. It’s one of the reasons I am not a fan of short daily for most patients … though it IS good in the original guise that George Ting used it for in Mountain View (Ca.) those years ago … for the patients with narrow volume windows and bad hearts whose hearts do not well tolerate the 2 or 3 day breaks associated with conventional dialysis. But, that’s another story.
Now, despite switching to nocturnal, you have done so after all RRF has gone. It won’t come back – and all the wishing and explanation-seeking in the world won’t bring it back.
But, you have correctly noted that you don’t have thirst … why? … again, re-listen to the Webinar I gave on ‘Fluids’. If fluid is so slowly removed from the circulation (as it is in long, slow dialysis like nocturnal dialysis) and that removal rate is BELOW the rate of plasma refill (the rate at which the body can, from its’ fluid stores in its’ cells and from extracellular space), then the blood volume does NOT contract during dialysis.
It is blood volume contraction that drives thirst.
It is blood volume contraction that, by driving thirst, sets up the next big weight gain … and then need to again push for extra fluid removal on dialysis … and more blood volume contraction.
It’s a merry-go-round.
Finally, re the Critline™ – of course I am familiar with that! … and the nurse was right (to a point). The Critline™ has been useful if only to show us that most patients are chronically over-volumed. It seems that you were … by 0.9kg. And, when taken off, you breathed better – you said so.
I don’t quite agree that … “no matter what a person’s size, the circulatory system can only hold and safely remove about 2.0 per treatment without affecting the heart etc.” – but, I suspect you may have misunderstood her.
If she meant 2.0 (as in 2kg or 2litres) … and, I suspect this was your interpretation … then I beg to disagree with her.
If she meant 2.0% of dry weight … then I am very comfy with her comment. 2% of 150kg is a very different kettle of fish from 2% of 40kg.
Now – back to my weeks’ leave!
John Agar
Thank you Dr. Agar. Your answer makes perfect sense. Dan
Dan
I suppose I should add one single additional paragraph to the answer I gave you regarding RRF and nocturnal haemodialysis (ie: long, slow, frequent regimes). This regards the question of whether NHHD does (or does not) allow for the preservation of RRF.
As I said in my previous answer(s), there is good reason to suspect that NHHD should allow for the relative preservation of RRF - just as PD is known to do.
But … and this was implied but not stated in my previous answer(s) … this assumes that a patient ‘transitions’ from CKD5 or a failing transplant directly into NHHD and does not spend significant time on conventional haemodialysis during which time RRF might be expected to wither away quite rapidly.
Unfortunately, many NHHD patients only train for and begin it after a time (often prolonged) on conventional programs during which RRF is lost … for the reasons I gave.
To sustain RRF on NNHD then, if indeed RRF is sustained (as I suspect it is - though as yet we have no proof of that) … see my previous answers … then NHHD must be instigated before RRF is lost in a conventional program.
As I have said - once lost, RRF is gone, and all the wishing (and better dialysis) in the world won’t bring it back.
John Agar
Hi Dr. Agar,
What percentage of patients in your program go straight into nocturnal txs? I feel that competent training is everything, and as long as that is in place, patients could certainly go straight into nocturnal txs. thus avoiding the pitfalls of barely adequate txs. In the U.S., nocturnal txs are portrayed as the “boogie man” tx., causing patients to believe that nocturnal is only for more experienced patients, and creating a fear that it is too difficult to accomplish. Of course, nothing could be further from the truth. From my very first noctunal tx, I was smiling ear to ear like a Cheshire cat at how easy and comfortable it was, yet at the same time, a deep grief came over me at how long I had been denied this compassionate modality. I try to counsel patients now, don’t delay getting into nocturnal txs- the sooner you do, the better you will feel!
Jane
We began by transferring patients from our satellite facilities into our home program - a program which is, for our home patients, a fully nocturnal (8-9hrs), through-the-night, sleep-on-dialysis and home-based, average of 5 nights/week program. We do not have, nor have encouraged nor striven for centre-based NHHD programs in Australia … this is true except for a small unit in Nambour, Queensland which has pioneered that format here with only modest success and/or uptake. To date, however, we prefer to embrace home as home and not home as a facility. Our patients seem to do so too. maybe that’s how we ‘put it to them’ … but, whatever …
In my unit, most of our NHHD patients first came into our NHHD training program by selected transfer from facility care … and, incidentally, to link with Dan’s question on residual renal function (RRF), that meant that these patients had little or (usually) no RRF left on board.
Once we had trained and home-installed as many of our facility-based patients who were keen to (or persuaded to) move to NHHD, we began to encourage CKD4-5 (see below). Some home-suitable facility-based patients elected to stay in our facilities (as was their choice) though many of these have eventually moved to home NHD due to ‘peer pressure’ from their previously facility-based dialysis patient friends who, having realised the value of a well-supported home program and after becoming comfortable and secure at home, then told their facility-stuck friends that they should 'get a bit of this NHHD thing’.
Once we had trained our facility-based bunch of ‘suitables’, we began to work on our CKD4 to CKD5 patients. There was a second, smaller group – those with failing transplants – and these were included in our blanket education program that ‘home is best’ and that ‘facility care is there to help if you cant help yourself at home as the first choice and preference’.
We clearly and rapidly recognised that these two groups would be the future major backbone to sustain the program into the future.
We start our education program at eGFR 25. We ensure AVF insertion is underway eGFR 20 and so that there is 6 months+ to allow AVF maturation in most patients. We will always be caught out by late referral or acute chronic, rapidly progressing diseases, but these are not the majority of patients.
We have a full-time dialysis educator who, along with our nephrology team, encourages home if at all possible - be it home PD or home HD - and we have sustained a reasonable balance between the two, I think, though HD does exceed PD in numbers most of the time.
I said ‘if at all possible’ … and that is an important statement. A well supported and funded home program MAKES home dialysis possible for far more patients than most think, just by being there and by being active and supportive.
Now, our patients all come from CKD (most) or failing transplants (a few). I cannot think of a facility-based patient who has moved across now in the last 2 years of so … all that can (or will) come from our facilities, have probably done so by now. We just try to ensure that no NEW patients capable of home end up at the facilities and not in the home training program.
In Australia, of the 32 units nation-wide with >100 patients, one (not my own, I may embarrassingly add here) has 66% of their total patient population at home with 20 % of their total on HHD, 40% of their total on HPD and 33% on facility-based HD.
The average for these 32 largest (>100 patients) Australian units is 32% home with 10% HHD and 20% HPD and 70% facility HD.
My own unit currently has 32 of 112 HD patients at home on NHHD = 28% of our HD while we have a further 20 home PD patients. While we have the highest % of home HD in the country at 28% of all out HD patients, our PD isn’t up to national scratch. This is an issue for us to address – and we are trying to do so. We have only 16% of our total on home PD (less than than the average for the biggest 32 units) but 24% of our total patients (HD and PD) are at home on NHD (greater than the biggest 32 units average). 40% of all our patients are at home. But, clearly, this is not nearly as impressive (I blush to admit) when compared to the most aggressive home unit in the country (a New South Wales unit) whose figures I gave above.
Most of us train STRAIGHT to NHHD from CKD4-5. We have 3 training chairs with a 4th accessible. We commonly have a waiting list for training. We train for 5 hours 4 times a week on M/T/T/F. Our training time is usually 4 weeks (some go faster, some slower … training is at the patient’s speed) but most are home in <6 weeks. We occasionally do a week or two of daytime home HD when patients 1st go home but prefer to go direct to overnight runs in most patients. We have 24 hour technician and nurse support (phone) which seems to work well.
But, back to your Q …
The best way to secure home, ensure its acceptance, prevent discouragement and get the best outcomes is for patients who are home-suited to NEVER SEE THE INSIDE OF A FACILITY … EVER!
Now, you and I know that is easily said but not so easily achieved … but it should be our goal.
Without that as the goal, patients will end up drifting to, being parked in, or simply becoming resigned to facility care. I, for one, do not believe that is good dialysis practice.
However, we cannot escape from the fact that, at the moment, many (and even in our best experience, most) do and will need facility care.
But … those that can go home should go home. We need programs that facilitate that!
Here … we fund and incentivise home dialysis over and above facility care. As it should be. Facilities should be the back stop, not the first stop.
So … the short answer to you question … as many of the CKD population as can go home, should go home.
And … that comes down to a robust pre-dialysis education system and a critical mass of home patients crying out, loud and clear … Home dialysis is the best dialysis you can get … so, do it.
And it is up to us - the professionals, to provide the where-with-all to allow that to happen.
John Agar
[QUOTE=John Agar;18865]A short answer to your dialysis journey, Jane, might be this … but, first, please re-read my initial answer to Dan as the answers to most of your issues are contained within that 1st answer.
You started dialysis with, probably, a residual renal function (RRF) equivalent to an eGFR of maybe 8-10 ml/min. Let’s assume that.
Things remained stable on the fluid front for you for quite a long time, maybe longer than many/most other HD patients are as lucky to have enjoyed as you were.
You had a urine output, sustained by your RRF, which, though it was dwindling slowly from your base disease (largely unbeknownst to you), was still giving you some leeway with your fluids through those 1st two years.
Then … zam! … your machine changed and the sodium profile was reduced from 140-145 to 134-139 in your new machine.
The sodium concentration of the dialysate is used to ‘drive’ or, to use a word you tend to like (but I tend not to), to ‘script’ the movement of water.
A sodium level (concentration) in the dialysate that is ‘set’ to a lower concentration (say, 134-139) than that of your blood concentration (which is more like 140-145) will drag water from your circulation, across the membrane into the effluent and away. A sodium level of 140-145 tends to be in more balance with your blood.
NB: There was a time when there was a fashion (one I do not personally like) of ‘sodium ramping’ … but let’s not go there – it’s NOT easy ground and it’s not, in my view, a good practice to adopt except (maybe) in rather rare and special circumstances that are NOT useful to explore in these pages. I know some might disagree with me on this – and that’s fine – but I am sticking to my view!
When you were changed to a machine set to a lower sodium, water was sucked from you, your BP dropped, you cramped, you became hypotensive and symptomatic … and, after re-reading my 1st explanation to Dan (see above) you will now realise that your native kidneys experienced (as you were) a reduction in perfusing blood volume … your kidneys were being made ischaemic (lowered perfusion, blood flow, and oxygen delivery) as a result.
So, down went your RRF! … and once gone, it won’t return.
Your volume was ‘re-set’ lower but, in the re-setting, you lost your RRF and the flexibility of a urine output and of fluid intake freedom that allows (again, see my 1st answer in this thread).
This is the way with most haemodialysis patients … and most don’t have the luxuries of urine output and fluid freedom that you seem to have enjoyed in those early months … so, in a way, you can count yourself blessed that your RRF ‘kicked’ for as long as it did.
As I also made the point in my 1st response to this thread that short daily does exactly this, too. It’s one of the reasons I am not a fan of short daily for most patients … though it IS good in the original guise that George Ting used it for in Mountain View (Ca.) those years ago … for the patients with narrow volume windows and bad hearts whose hearts do not well tolerate the 2 or 3 day breaks associated with conventional dialysis. But, that’s another story.
Now, despite switching to nocturnal, you have done so after all RRF has gone. It won’t come back – and all the wishing and explanation-seeking in the world won’t bring it back.
But, you have correctly noted that you don’t have thirst … why? … again, re-listen to the Webinar I gave on ‘Fluids’. If fluid is so slowly removed from the circulation (as it is in long, slow dialysis like nocturnal dialysis) and that removal rate is BELOW the rate of plasma refill (the rate at which the body can, from its’ fluid stores in its’ cells and from extracellular space), then the blood volume does NOT contract during dialysis.
It is blood volume contraction that drives thirst.
It is blood volume contraction that, by driving thirst, sets up the next big weight gain … and then need to again push for extra fluid removal on dialysis … and more blood volume contraction.
It’s a merry-go-round.
Finally, re the Critline™ – of course I am familiar with that! … and the nurse was right (to a point). The Critline™ has been useful if only to show us that most patients are chronically over-volumed. It seems that you were … by 0.9kg. And, when taken off, you breathed better – you said so.
I don’t quite agree that … “no matter what a person’s size, the circulatory system can only hold and safely remove about 2.0 per treatment without affecting the heart etc.” – but, I suspect you may have misunderstood her.
If she meant 2.0 (as in 2kg or 2litres) … and, I suspect this was your interpretation … then I beg to disagree with her.
If she meant 2.0% of dry weight … then I am very comfy with her comment. 2% of 150kg is a very different kettle of fish from 2% of 40kg.
Now – back to my weeks’ leave!
John Agar[/QUOTE]
Hi Dr. Agar,
I have only just now gotten the time to come back to your reply here and study it out as opposed to skimming through. Please correct me if I am wrong, but what I think I hear you saying is, when my machine was taken for maintenance and came back with the lower conductivity setting, there was a greater pull than my system could handle causing hypotensive incidents that caused my RRF to diminish faster in time?
To better understand what you are teaching here, could you give me brief definitions for sodium modeling (or ramping as you call it) and for conductivity? Certainly, I can look these terms up, and have in the past, but I would like to hear your description, as well as how the conductivity rate affects the sodium modeling rate, thus the fluid pull? Because when my machine was taken away for maintenance, I had said that the machine was now reading a lower conductivity rate (not a lower sodium modeling rate) of 13.4 - 13.9 when it had previously been at 14.0-14.5. I believe this was due to an internal calibration by the tech. My limited understanding through reading a number of articles and through the experiences of other patients, is that some patients can not tolerate a too low conductivity. It was not the sodium modeling rate that changed, but the conductivity rate. So, I would think it is the conductivity rate that affected the sodium modeling rate. Sorry if this is confusing as I am doing my best to explain what I observed to you.
When I was again put on a machine that was at the 14.0 - 14.5 conductivity rate, I was fine again and back to being able to remove a goal of 3.5 with no problems.
When I was transferred to my next unit, this is when I had a problem again. At the new unit, not only was I put on machines with differing conductivity rates since they switched our seating around, but I was also given an entirely different sodium modeling scrip. It was at this point, that I had one incident after another and the only way I could get around it was to remove a smaller goal.
So, although I do not fully understand how sodium modeling affects conductivity, or vice versa, and would appreciate an explanation of this, do I understand you correctly that it was the harsher settings of the machine that made it impossible to pull off my 3.5 goal and eventually brought my RRF down? I know you said there is natural reduction of RRF going on, but were the harsher machine settings the primary cause?
Dear Jane
In the early days of dialysis, the ‘conductivity’ of the earlier proportioning single pass dialysis systems was measured by the chloride concentration of the dialysis fluid. This dialysis fluid, now commonly called the ‘dialysate’, also in earlier times, originally referred to the effluent removed from the artificial kidney after dialysis against the patients’ blood and not, as it tends to now be used, as the pre-prepared or mixed final fluid formed before dialysis and which is brought to the patients’ blood at the dialyser.
The electrical ‘conductivity’ of a solution is a measure of the ability of a solution to transfer (or conduct) an electric current. Conductivity can be used to measure the concentration of dissolved solids (electrolytes: like sodium and chloride ions) which have been ionized in a solution such as water.
In dialysis, we need to know that if we are bringing a patients’ blood into contact with a solution – like the dialysate – the solution (dialysate) has a known and predictable electrolyte mix.
We measure the dialysate conductivity to ensure that.
Measuring the ‘conductivity’ of the dialysate became the routine way by which the dialysis fluid (which we now call dialysate) could be checked for its chemical ‘correctness’ before bringing it to the blood contact point at the membrane.
Early on, chloride was easy to measure and, so, there was a conductivity ‘meter’ on the dialysis machine which ensured the chloride concentration stayed within close boundaries. It was determined that if the chloride ‘mix’ (or dilution’) resulting from the single pass systems’ proportioning pump (the part of the dialysis machine responsible for mixing dialysis-grade water with a chemical concentrate) was OK … the other electrolytes of the dialysate would be too and the ‘proportioning system’ was working within specifications.
In the early days, the conductivity was ‘set’ … and that, pretty much, was that.
Then, in the 80’s and 90’s, researchers became interested in being able to modify (or change) the conductivity but, not to change the chloride concentration but to alter the sodium concentration … for, as I teach my students, “whither go’eth sodium, go’eth water!”
If the dialysate sodium could be lowered, then sodium would pass across the membrane from the blood into the dialysate as the two solutions ‘equilibrated’ … and water would be dragged across too, by the movement of the sodium … ‘whither go’eth sodium, go’eth water’. This would lower the water volume of the patient – and reduce dry weight and BP.
And so, over time, the term ‘conductivity’ morphed from a term originally based on the chloride concentration of the dialysate to a term which described its’ sodium concentration. Now, when people talk of conductivity, they are more likely to mean the sodium concentration and not the chloride concentration.
Researchers realised that if the sodium concentration could be changed, up or down, the volume of body water could be also modified, down or up, as a result.
Lower the dialysate sodium … and drag off more water from the body as it followed sodium from the body to the dialysate … and … lower dry weight and lower the BP … etc.
Elevate the dialysate sodium … and add more water to the body as it followed sodium to the body from the dialysate … and … raise dry weight and raise the BP … etc.
So … the concepts of sodium ‘adjustment’ or ‘modification’ through (during) a dialysis treatment became of interest. It became possible to either pre-set a desired sodium concentration at the start of dialysis or even to alter it during the treatment. This became known as the process of ‘sodium modelling’ … where a predicted outcome for body water, blood volume and their resulting effects on BP and dry weight could be ‘modelled’ for any particular patient or situation. This could be done in a stepwise fashion (‘stepped’) or in a more continuous, progressive manner, like a slope (or a ‘ramp’).
Sodium modeling has largely fallen out of favour. I certainly don’t get very excited by it! We rarely consider it and don’t practice it. Most don’t. Some still potter around with it – and good luck to them – but my interests lie elsewhere … by providing better volume and BP control through modification (and prolongation) of dialysis time and frequency.
Now, we could get a lot more ‘intricate’ than this – but, Jane, I see no point and it will serve most (even you) little purpose to do so. I don’t think it will be helpful to others for us to extend this conversation further. If you are keen to do more of your own research, you are welcome to do so. However, this is as far as I think it is sensible to go on this topic here. Whether any changes that were made – intensionally or otherwise – to the sodium concentration of the dialysate of your machine(s), way back then, had anything to do with – or nothing to do with – your co-incident loss of RRF is impossible to now know and, if I might be candid, is of little relevance to your here and now.
Let us (and you) now move on from here.
John Agar