Acidosis and other stuff

Hello Dr Agar,

I hope that you are well, not too busy and life is treating you grand. Here is another question for you if you don’t mind answering.

Please could you explain the significance of acidosis in renal failure and the affect it has on the constitution of the bone mass/density? Also, can mineral bone disease affect just one part of the body significantly more or is it a general decline on the whole of the skeleton?

I have just been given some bicarbonate tablets (500mg 2x per day) why would they give me these and will it not affect the total sodium tolerance intake. I was told to keep an eye on blood pressure but it hasn’t changed still around 135/78. I’m not on any dietary restrictions at the moment?

Thank you for your time.

Yours truly,

I think acidosis is an ‘undervalued’ issue in chronic kidney disease (CKD) and renal failure – in part because its effects are commonly subtle and do not cause ‘obvious’ symptoms and in part because it kind of falls last in line for treatment with the other aspects: anaemia and iron management, control of blood pressure (hypertension), lowering of lipid (blood fat) levels, correction of calcium and phosphate imbalance, parathyroid hormone (PTH) suppression with vitamin D and/or calcium mimicking agents like cinacalcet, the management of the accelerated cardiovascular complications of CKD and a host of other seemingly – or in reality - more ‘pressing’ issues.

By the time all those (seemingly) more urgent issues are treated – and the poor patient is already swallowing dozens of pills a day – the treatment of acidosis just seems one step too many, or one additional step too hard.

That is NOT to say that that is a correct approach – just a practical and pragmatic one … especially considering that the only effective means of reversing acidosis (other than by good dialysis) is by using agents like sodium bicarbonate (NaHCO3) = mothers baking soda - but in capsular form. You will understand why NaHCO3 is packed into capsules if ever you tried to swallow a neat spoonful of baking soda!

But … note the word ‘sodium’ or, using kitchen-talk, ‘soda’.

NaHCO3 enforces a sodium load. A sodium load is counterproductive for patients already struggling with the control of their blood pressure, or who have left ventricular (LV) failure or LV overload states (= most patients), or for those who are struggling to control thirst and inter-dialytic weight gain from fluid overload.

For these patients (and it IS the majority), adding yet more sodium to chase and reverse what many think the lesser evil – the effect of chronic acidosis on the metabolism of bone – can be one straw too many.

For those where volume is not an issue (some), or where blood pressure is easily controlled or not an issue (a few), or where the LV is still strong and unthickened by LV hypertrophy … for those, the treatment of any identified acidosis with NaHCO3 is a welcome luxury – and should be embraced.


Well … acidosis is NOT as innocent an issue as some would hope it to be.

The proper terms for the acidosis of CKD is metabolic acidosis and it occurs when the body is either producing too much acid … as can occur with diabetes when it goes haywire and out-of-control and a state called ketoacidosis occurs; when excess lactic acid is made (eg; in long distance runners, or with certain medications taken either as prescribed (eg: metformin in CKD4-5), or by overdosing with substances like salicylates; or when the kidneys are not removing enough acid from the body – as occurs in advanced CKD.

Acidosis is probably more of an issue for patients with CKD than for dialysis patients for GOOD dialysis corrects acidosis well and removes (or buffers) excess acids efficiently. In simple terms, buffering means neutralizing: add alkali to acid and the two cancel each other out, trending to a neutral pH (or a neutral acid:base balance). Note: bad dialysis does not achieve this adequately!

The chronic, persistent, but usually low-grade acidosis that accompanies CKD subtly alters the composition of bone. This is perhaps most evident in children with CKD where the bone is still growing, lengthening and strengthening: perhaps it is in children, especially, that reversal of acidosis should take a more primary place in the treatment matrix.

Chronic metabolic acidosis changes the ionic composition of bone, reducing bone concentrations of apatite, sodium, and potassium. The genes that encourage osteoblast (bone-forming) activity are suppressed while, conversely, osteoclast (bone-reabsorbing) activity is increased. Further, growth hormone, a hormone that helps to encourage bone growth and guides its ordered structure, is also suppressed.

At the end of the day, if acidosis is present and there is room to treat it - sodium loading in mind – then it should be treated.

Shaymon … if you blood pressure is good, your heart healthy, and your volume state manageable yet a chronic metabolic acidotic state has been identified, your physician is on the ball, on the money, and on track.

I agree with him – treat! Sadly, though, such a step is not easily do-able for the majority of patients. You seem, possibly, to be among the lucky few where NaHCO3 can be added in … and to your benefit … as long as volume, BP and other down-sides to NaHCO3 treatment don’t flare their nostrils at you.

Finally, re your question … ‘patchy’ or ‘widespread’?

The effects of a chronic metabolic acidosis are widespread - affecting all bone. The effects of PTH bone disease are not always so. This is a key difference between the two major bone-centric complications of CKD. But again: metabolic acidosis affects all bone.

I hope that this has helped to answer some of your questions.

Hello Dr Agar,

Thank you for replying so promptly to my question. Your answer has been very informative and helpfull. After what you say I shall consider myself one of the luck few at the moment, long may it stay that way. Although at the hospital they are not quite so positive…we shall see.

Again thank you Dr. Agar


Dear Shaymon

One thing I may not have made clear is the lack of ‘instant gratification’ gained or expected from the reversal of metabolic acidosis … by that I mean that most patients commonly seek or expect some tangible ‘outcome’ from a treatment - some tangible benefit in the way of either symptom relief or an ‘I feel better now’ response.

Any benefits gained for either nutritional status and/or to bone metabolism are slow, intangible benefits. They happen, as it were, behind the scenes … in nooks and crannies of our organism, where changes occur slowly and do not trumpet any outward evidence of change.

That said, if the reversal of an identified state of chronic metabolic acidosis can be achieved (as it can be in some) without destabilizing blood pressure control or volume status and without adding to the factors which increase the ‘burden’ (or load) on the left ventricle, then I think it should be encouraged. But … while both the structure of bone and overall protein metabolism will be advantaged in the longer term by so doing, this will not be a ‘noticed’ benefit … just a ‘background’ benefit.

As for the available ‘versions’ of NaHCO3 … here, we only have a common-or-garden version of NaHCO3 on the market = mother’s baking soda (840 mg) packaged in a gelatin capsule. While it is as cheap as chips, it is a rather unsophisticated formulation.

In Europe, there are at least 2 x versions of enteric-coated NaHCO3 (Nephrotrans and Bicanorm) - both purported to be more effective and less associated with any side-effects. However, my experience tells me that side-effects from NaHCO3 - other than those associated with blood pressure, volume and left ventricular load issues - are rarely if ever seen.

The gelatin-capped NaHCO3 - as available here in Australia - is likely to be less effective as less HCO3 will be available for absorption as most is ‘wasted’ on simply neutralizing the acidity of normal stomach secretions.

But … that all verges on pharmacology = not a strong suit of mine!

Hope that’s of some use.

Hello Dr Agar,

I suppose really it’s like trying to repair a building with sticky tape rather than rebuilding its foundations. I never thought about the ‘instant gratification’ factor. I suppose with bones, repairs of any kind will take time just because of what they are and how they are constructed. How in that case would the Neph determine that the damage has (eventually) been repaired/restored, would it be by parathyroid hormone (PtH) level screening or would it have to be by x-ray/scan? Also what would be the physiological signs that thing are back as they should be considering this is a background issue rather than a prevalent one?

I apologise for coming back with more questions but the answer and adage you gave just provoked some more, also I find this rather interesting… I can just imagine the dinner conversation with my kids, them saying that my doctor fixed me with baking powder.

Thank you for your time


Yes … bones do take time. And, we are not as good as you might think we are (or should be) at understanding dynamic bone changes nor do we know a lot about any other than ‘blunt’ methods of monitoring bone indicators of change or ‘improvement’ with treatment.

Much is said and written … correctly, mind … about PTH, alkaline phosphatase and ‘like’ bone indicators and their relevance to bone in CKD but, in truth, they are still very rudimentary measures, they react (and thus only allow us to react) ‘after the fact’ and they only give us the equivalent of an unmagnified view from space of Planet Bone – without the ‘focus-in’ function that IT engines like Google Earth give us. Would that we were able to focus more acutely, but sadly we can’t.

For example … to understand glomerular disease, we needed to look into the body, inside the kidney. We needed to get tissue, to magnify it, test it, stain it, seek electron microscopic changes magnified up 10’s of 1,000’s of times. A blood pressure machine, a urine sample looking for protein or blood, and/or a raft – however complex – of blood tests diluted by, added to, mushed about and metabolized by every organ we have – these paint a broad-brush picture … but, in reality, yield far less information, singly or together, than we need to know to really understand glomerular disease.

To better understand glomerular disease, we needed glomeruli. So … to understand bone disease, we ideally need bone!

Those who have ever had a bone biopsy will tell you ‘that may have been my first, but it will also be my last’! Bone biopsies hurt. It’s the main reason why we know less than we otherwise might about bone metabolism – slow as it is – and about the laying down and reabsorbing processes that are the dynamic of bone. That is not to say we are clueless – far from it – just that we still lack sharp, real-time, reliable markers.

Xrays, CTs, MRIs and bone scans (nuclear or dexa) are like looking at New York from a plane at 30,000 feet and feeling, somehow, that you now have a clear picture of what lies below, in all its bustling, frenetic detail. You know that that is not possible – unless you have a screw-down (or up) lens that allows magnification (GoogleEarth-esque).

Even then, the view would be two-dimensional. We need to see depth, too. We need to hold, turn, explore - like the sights, sounds and smells of a city add so much to a birds eye view, so we need to get up close and personal with bone to know it in all its amazing complexity. Bone is not just a bunch of pillars of calcium and hydroxyapatite. Bone lives, breaths and metabolises. It is a still-to-be-conquered frontier. So … we have much to learn and a long way to go to really understand bone.

There is stuff ‘coming’ … as only one example, FGF-23 (FGF = fibroblast growth factor) has opened up a very promising line of research. I say (just) a little more about FGF-23 in the plain language medical student text I wrote for Australian medical students ‘Nephrology Made Easy’ – which can be accessed on-line at - though this is probably more than an audience at this site needs or wants.

I have also dealt with some of this ‘bone’ stuff in earlier posts … one from ‘Jane’ about ‘elevated alkaline phosphatase’ surfaces in memory … so it may be worth scanning back over previous thread headings for bone-related responses.

At the end of the day, we use blunt markers of bone activity and, as such, we tend to identify – at best – change ‘after the event’. Then, when we react, the reaction comes often well after the horse has bolted. In an attempt to then ‘bring bone back’ to the centre - what do we do? Overshoot … but in the opposite direction.

One day ….

Dear Shaymon

Since writing my responses to you, I have received a critical, and occasionally stinging attack by direct email at this site from someone (unidentified) who disagrees strongly with my statement that ‘the treatment of metabolic acidosis in CKD is only an option for the ‘lucky few’’ and that most nephrologists still leave it as one of the last among the long list of CKD ‘effects’ to treat.

First, and on reading his/her comments, I would say that he/she is quite correct in his/her criticism(s) of my approach and of my answer – though perhaps a little less vehemence might have made a nicer read, at least from my point of view.

It is always difficult, when putting oneself ‘out’ on the Internet (as I agreed to do for Dori and her team at HDC) to answer any/all questions from all and sundry on almost any subject. Occasionally (and I hope it is only occasionally) I will get it wrong. I try to be as majority-view as I can … except where I state otherwise - and then I try to identify my diversion from the views of others.

This time, I have unwittingly but clearly exposed a raw nerve. Furthermore, the emailer is right to take me to task and is right in his/her criticism and the points he/she has made.

I am also grateful that he/she did this through a private email and did not subject me to ‘the glare of the headlights’ at the Q&A site.

The emailer points out – rightly – that while current dogma dictates that what I answered you is the current view, that does not make the current view (or dogma) right!

As he/she pointed out to me, and I affirm here, there is little (if any) factual evidence that sodium overload does result from the administration of NaHCO3 … indeed, that’s true … and that the dogma that inhibits appropriate treatment of acidosis is just that - dogma … again true.

I have long been one known to challenge dogma – my views that challenge the dogma of Kt/V are epecially well known – but on this occasion, I have been hoisted on my own petard as a ‘dogmatist’ in my own right! Touche!

I accept the criticism made and applaud the correction – and my education in the process, However, that does not escape the fact that it does remain the majority view (and, as I agree with the emailer, this is incorrectly so) that reversal of the acidosis of CKD tends to take a ‘last in line’ place in the management priorities.

That this should change – and fast – and that the science inhibiting that change is flawed (if science at all), is not in dispute.

As I also said in my response to you – I agree with your nephrologist that acidosis should be treated. At least, I think I said that.

However, my remark ‘treatment is only an option for the lucky few’ was clearly a mis-statement.

Perhaps I should have said that you, Shaymon, are one of the ‘lucky few who are seeing a nephrologist who treats what should be treated’ and what i missed saying - but should have - is that 'the treatment of metabolic acidosis has far less, if any, of the purported risks - contrary to accepted dogma’.

I certainly do not want to get into a slanging match at this site. I must say that if that were to occur, I would seek to withdraw completely from any further attempts to answer questions and leave that to others better qualified. The use of the private email facility was appreciated.

However, as the emailer was correct, I felt it right to offer this correction. I trust this will serve to mollify the emailer as well as correcting my earlier response.

Hello Dr Agar,

Sorry for not coming back to you on this but I have been unwell for the past few days (nothing to do with CKD), just one of those nasty bugs mother nature throws at you some times.

I too would not want to provoke an open slanging match on this (or any other forum). I asked you a question of which you gave me an answer in the spirit that makes this site so informative and to others essential. I also accept the terms and conditions in the site’s disclaimers. Further more you can only answer the question with the information you have been given and cannot (most importantly) give a one-on-one personal advice because you don’t have the patient’s individual record or knowledge of their health history.

In your reply I understood the meaning of your statement about the ‘lucky few’ and about those that can be treated with Bicarbonate for acidosis, and accept that is your opinion, after all that is what I asked for. The technical niceties of Nephrology I of course leave to experts like you and the e-mailer to discuss and agree/disagree with, but for me rest assured no harm done in my case.

I am pleased that the last Neph I saw picked up on this and gives me confidence that they are in fact looking after my well being, this being confirmed in your answer to me.

I am sure like many others find your answers helpful, informative, and also in a language that we all understand. You are asked your opinion which you give freely and without bias…long may this continue.



Oooh, I’m really glad to read a post on this because I’ve been taking Sodium bicarb (8 tablets a day!!! Urp!!) for several years now. I had just returned from a 3 mile walk, feeling healthy and virtuous, and my neph’s nurse called to tell me that she had just received my latest lab results, and my potassium was suddenly high (at 6). I knew what high K can cause, so I was very nervous. After some to-ing and fro-ing with the neph, it was decided that I’d start taking sodium bicarb and retest in a few days. Well, that strategy worked, but I still have trouble controlling my K level. Most of the time, it is barely within “normal limits” and is as often as not a percentage point or two over.

I read the information pamphlet that came with the tablets, and I saw that this is a treatment for acidosis, but what is the link between acidosis and high potassium? My neph has never said the word “acidosis”, so I am confused. Can you educate me once again, Dr. Agar?

I am very sorry to hear that anyone corresponded with you in a less than respectful tone. I appreciate the time and effort you take in using your personal time to answer our queries, no matter how insignificant they may be, and you deserve to be treated with gratitude and kindness.

Central to the whole sodium and potassium story is a teeny-tiny molecular ‘baling’ pump … known as the sodium potassium ATPase pump (the Na/K ATPase pump).

The NaK ATPase pump is made up of a specialised protein molecule - a protein which is located within the surrounding membrane of all our cells … if you like, the cells’ skin. The Na/K ATPase pump is driven by (energized by) a phosphate-dependant enzyme system called adenosine-triphosphate (ATP).

Note, here, as an aside, that phosphate is of vital importance to us (as well as being a potential ‘toxin’, if accumulated in excess, in CKD) - for phosphate drives many (if not most) of the energy-requiring systems of the body through this amazing energy-giving powerhouse, ATP.

In all land-based organisms – yes, in man, too – the sodium level (the sodium concentration) in the tissue fluids outside the cells is normally higher than the sodium level (concentration) inside the cells.

On the other hand, the concentration of potassium inside our cells is normally higher than the potassium concentration of the fluid outside our cells – this 'outside-our-cells fluid (the extracellular fluid) includes the tissue fluids that bathe our cells as well as the blood itself. About 98% of our potassium is held inside the cells and only 2% is outside, in the extracellular fluid and blood.

Without this amazing little energy-requiring pump, sodium would flood into our cells from the extracellular fluid down its concentration gradient. Water would follow (whither goeth sodium goeth water) and our cells would swell, burst and die.

Quite opposite to the way it is with potassium, the concentration of sodium outside our cells is normally about 10 times that of the concentration inside our cells … and, yes, it is meant to be that way.

Outside our cells, we are sodium salty. Inside our cells, the sodium salt concentration is low. This is essential for normal cell function.

Outside our cells, our body fluids are potassium-poor. Inside our cells, we are potassium-rich. This is also essential for normal cell function.

Without the Na/K ATPase pump, potassium would pour out of our cells into the extracellular fluid and the blood. The blood potassium would then rocket upwards. The Na/K ATPase pump ensures that this does not happen.

So … this amazing teeny-tiny pump is constantly baling sodium out of our cells (like a sailor might bale water out of a sinking boat to keep it afloat) while it holds potassium inside the cells – where it is meant to be – and prevents it from leaking out.

This tiny protein pump is one of the most important biologic systems in the body and uses a staggering 25% of the caloric energy intake of the body to sustain it.

Now … when acidosis happens along, a new problem arises.

As the pump also pumps hydrogen ion (H+) from the cell, in situations of acute acidosis (= too much H+), - like diabetic ketoacidosis – or in situations of chronic acidosis – like CKD – the pump preferentially tries to pump H+ out of the cell and, at least for the moment, ‘kind of forgets’ about maintaining the potassium gradient. While it gets busy with handling hydrogen (H+) ion, it (kind of) forgets that it is supposed to maintain a very high potassium level inside the cell and ‘loses its way’.

Potassium then begins to leak out of the cells into the extracellular fluids and the blood … and, a high blood potassium is the result.

Acidosis, therefore, always tends to promote a high blood potassium level.

Correcting the acidosis by the administration of bicarbonate ‘buffers’ (ie: balances or neutralises) the excess hydrogen (H+)ion.The pump stops spending all its energies on H+ and happily returns to sustaining the sodium and potassium balance again - sodium outside high and potassium outside low : sodium inside low and potassium inside high. Potassium then stops leaking out of the cells into the extracellular fluid and blood, and is pumped back into the cells … where it is meant to be.

Phew! … that’s a very complex little bit of physiology in (hopefully) some understandable language.

While you may have to read it a couple of times to get it clear, I hope that that helps.

Oh, that’s just fascinating, it really is. That explains a lot! Thank you! It never ceases to amaze me just how complex we human organisms are.

Dr. Agar,

I am very grateful to have found this forum and appreciate the information you are providing to dialysis patients like myself!

I am at stage 5 CKD and set to begin peritoneal dialysis in a few weeks, and I have been trying to read up on acidosis in renal patients. This was prompted by my nephrologist telling me that I was acidotic. Like Shaymon and MooseMom, I am taking sodium bicarbonate tablets (2 tablets 3x daily). In addition, my nephrologist also advised me to eat a 2-to-1 balance of alkalizing to acidifying foods, at least until I got on dialysis. She provided a list she had printed from a website, listing a number of major foods as either alkalizing or acidifying (the list appears to have originated from the Wolfe Clinic ( Just when I thought I had gotten comfortable with the renal diet, adhering to this list was a new struggle!

My girlfriend tracked down a cookbook in hopes that it would help us make sense of the alkalizing diet (The Amazing Acid Alkaline Cookbook,; the recipes are constructed to have an overall alkalizing effect. The book also provides a chart of foods, noting whether each one is alkalizing or acidifying. The information on these foods appears to be taken from another book, The Acid-Alkaline Food Guide, by Dr. Susan Brown ( Ultimately, however, this cookbook has proved to be more confusing for me than helpful.

Though the lists are generally in agreement (meats, grains, oils are acidifying; many fruits and vegetables are alkalizing), there are still numerous discrepancies between the lists. Looking to the Internet for more information has proved fruitless, as each new list I find contradicts all the others in some way. Further, the vast majority of alkalizing/acidifying food lists I find are on sites propounding what I would consider a naturopathic approach to medicine (which makes me hesitant to trust them at all).

Unsatisfied by my Internet search, I began searching in the academic journal databases subscribed to by the university library where I work. I have located some of the research on treating acidosis in renal patients with sodium bicarbonate. There were also a couple of studies mentioning the use of sodium citrates or potassium citrates as an effective treatment. (My nephrologist was recommending that I drink lemonade to help alkalize me, so now that makes sense.) Try as I might, I could not seem to locate any published research on dietary treatments of acidosis, as my nephrologist has advised. There is one unpublished study mentioned on the DaVita site: a team of researchers at Texas A&M led by Dr. Nimrit Goraya (2010) found that an “alkalizing” diet heavier in fruits and vegetables did slow down kidney injury in patients with kidney disease in early stages. Unfortunately, since I can’t read the study, I cannot access their list of which foods were alkalizing. I have been unable to contact Dr. Goraya so far.

So, my questions to you:

You mentioned that, short of good dialysis, the only effective means of acidosis treatment is sodium bicarbonate. Is the use of sodium/potassium citrates also an effective treatment for acidosis in renal patients?

Is there a strong research basis that would indicate I should control my acid load through my diet until I get on dialysis? After reading your explanation of the NaK ATPase pump, I am beginning to question an alkalizing diet even more. That is, if the pump is too busy with hydrogen to keep potassium out of the blood, and many fruits and vegetables can be higher in potassium…you see where I’m going.

Lastly, if there is a strong research basis for dietary treatment of acidosis, is there any sort of authoritative list of whether foods have an alkalizing or acidifying effect?

I appreciate you taking the time to read my terribly long post and questions. Thanks again for all the great info on this forum!


Re: Acidic v alkaline foods

Dear Casey

Thanks for your question. As far as I am aware, there is no certain recommendations or good research into the effects of ‘acid’ versus ‘alkaline’ foods in CKD … but this is probably a question best asked of our dietitian expert, LeeAnn Smith.

Here, we use our dietitians to answer curly questions like this … and I confess to less-than-useful dietary skills. I know that’s a cop-out, but it’s true. So … can I suggest you copy and paste the same question to her forum site. You will find it at the HDC site home page. LeeAnn is more likely to give a wiser (and more accurate) answer than I can on this topic.

Here, we tend to use sodium bicarbonate (NaHCO3) capsules … mother’s baking soda in a pill … as our alkalinizing agent.

NaHCO3 are cheap, easy to obtain, and work.

Sodium citrate can taste a bit yukky, I believe, while potassium citrate can be a bit harsh on the tummy – though both are used as alkalinizing agents for patients with recurrent UTI and both are valid alternatives to NaHCO3. I guess my hand is just better trained in writing scripts for sodium bicarbonate.

Casey: ask LeeAnn. I’d bow to her better knowledge here!