See : "Is an Increased Serum Bicarbonate Concentration during Hemodialysis Associated with an Increased Risk of Death?" Seminars in Dialysis vol 27 No 3 (May-June) 2014 pp 259-262

I have not the paper. If I will have it, I send you a copy

Thank you for the tip (fulltext is attached). It seems that the question of dialysate bicarbonate concentration is still unclear. The most studies focused on the evaluation of predialysis serum bicarbonate concentration. In my opinion, the important risk factor could be the rapid and extensive alkalinisation during hemodialysis. The commonly used concentration of bicarbonate bath is between 32-40 mmol/L.

We used concentration 32 mmol/L in postdilution on-line haemodiafiltration. The mean serum bicarbonate concentration before and after HDF was 23,4 and 28,3 mmol/L, resp. The postdialysis concentration perfectly corresponded to the dialysate bicarbonate (32 mmol/L) after corection on plasma water concentration (coefficient 0,93) and after taking into account Donnan coefficient (0,96).

Theoretically, if we used dialysate bicarbonate concentration 40 mmol/L, the postdialysis serum concentrations would be 35,7 mmol/L (after correction to plasma water concentration and Gibbs-Donnan equilibrium).

Thus, a patient who has a sufficient protein intake in interdialytic period and reduces bicarbonate concentration from 35,7 (postdialysis) to 20 mmol/L (predialysis usual value), the serum bicarbonate will increase about 15 mmol/L during 4 hour dialysis (with regard to KDOQI giudelines to achieve pre-dialysis bicarbonate concentration > 22 mmol/L). Is not such correction rate too dangerous? The intradialytic bicarbonate increase is achived together with retained acid anions elimination. Is the electrolyte movement between fluid compartments and distribution space of bicarbonate and various acid anions equal? Or may occur disequlibrium?

Don't look only to bicarbonate post-dialysis concentration: it is not enough ! Above all look at pH because post dialysis alkalosis (often mixed alkalosis) can lead to arrhythmias and mortality

I understand that pH is the crucial point for the complication as arrhythmia and bicarbonate is just the metabolic part of acid-base disorder. But in my experience there is no significant change in pCO2 (respiratory component) during haemodialysis or haemodiafiltration. Therefore, the intradialytic pH change is determined by the intradialytic bicarbonate change.

I would like to know, what effect has rebound phenomenon on postdialysis bicarbonate concentration.

Harris et al. (Harris DC, Yuill E, Chesher DW. Correcting acidosis in hemodialysis: effect on phosphate clearance and calcification risk. J Am Soc Nephrol 1995; 6:1607-12.) (fulltext attached, Figure 2) reported significant increase of serum bicarbonate concentration 2 hours after dialysis compared to end-dialyis concentration.

I understand the mechanism of phoshpate rebound, but what is the mechanism of bicarbonate rebound? I would expect the decrease of bicarbonate 2 hours after dialysis.

I download your attachement. I will read. Now I like to focus on pCO2 value througout dialysis session: as you have noted this value is unmodified. Hypocapnia is appropriate for pre dialysis metabolic acidosis, but it is maladaptive in the last part of session when metabolic acidosis disappeared (HCO3 doesn't cross haematoencephalic barrier and stimulus to ventilate doesn't decrease). Even if slightly Hypocapnia plus slightly hyperHCO3 yeld to abruptly alkalosis.

As concern bicarbonate rebound, take you in account acetate source of bicarbonate?

I have read the paper. It's very old. Nowaday dialysis is very different. See Qb and filter surface! However 4 -5 mmol/L of acetate are supplemental source of bicarbonate and could explain postdialysis increasing of bicarbonate.

As regard correction rate I like to underscore that gain of bicarbonate from dialysate is decreasing throughout dialysis session because delta-HCO3, i.e. HCO3 in dialysis fluid minus HCO3 in the blood,

- the driving force - decreases when HCO3 (in the blood) rises. Are you agree ?

ad 1) In our patients we reported the mean pH 7,38, pC02 5,37 kPa, bic 23,4 mmol/L before dialysis and 7,45, 5,5 kPa and 28,3 mmol/L after dialysis (postdilution HDF using bicarbonate 32 mmol/L). These finding are consistent with other studies I have seen. Therefore no portion of respiratory component.

ad 2) Thank you for the advice with acetate. I thought that the conversion rate is very very fast. It´s true that the study is old and the acetate concetration was high, but in my opinion in HD using low Qb and small filter surface should be the bicarbonate and acetate load decreased.

Do you know the rate of acetate conversion to bicarbonate? And do you know the plasma bicarbonate kinetic after dialysis (e.g. 0-30-60-120 min after HD) using dialysate containing acetate concentration 3 mmol/L?

ad 3) I agree that the diffusion gradient is the main driving force for bicarbonate (together with minor effect of ultrafiltration rate).

#1) There is not neither respiratory nor metabolic component: it is simply normal !

#2) I am not agree that conversion rate is fast , because it is not chemical, but metabolic (liver) reaction. one acetate --> three bicarbonate

1) o.k. no acidemia, no alkalemia, mild metabolic alkolosis (bicarbonate 28 mmol/L is above the upper limit of normal) with respiratory compensation, but 28,3 mmol/L was the mean, a lot of patients had bicarbonate more than 32 mmol/L.

2) one acetate --> one bicarbonate, one citrate --> three bicarbonate. The conversion is metabolic, but it is series of chemical reactions of Krebs cycle, it could be very fast. The question is how fast.

1) normal predialysis acid base and mild metabolic alkalosys post-dialysis. I full agree.

2) I don't know how fast

Bruno R., Plasma acetate and bicarbonate kinetics and intolerance to acetate during and after renal dialysis, 1984: ".....acetate decreased according to first order kinetics (half-life (8.82 +/- 3.42 mn)".

Do you have any experience with citrate acid concentrate (citrasate®)? After a few weeks using this concentrate I have noticed a higher frequency of hypotension and seizures at the end of dialysis or after dialysis. I think, one of the reasons could be triple load of bicarbonate compared with acetic acid.

I don't agree with triple load of bicarbonate. Compute accurately: in bicarbonate dialysis 3 acetate = 3 bicarbonate, with citrate dialysis: 3 citrate = 9 bicarbonate. For both 32 bicarbonate (35 from cartridge - 3 consuming by reaction with acid, acetic or citric, to generate Carbon dioxide). So in bicarbonate dialysis = 32+3 and citrate dialysis 32+9 that it is not 3 fold.

anyway bicarbonate load from dialysis bath is self limiting. .Increasing HCO3 in blood decreases HCO3 load from dialysate due to lowering driving force namely the difference between the abovementioned values.

seizures remembers both hypo Ca and Alkalosis. Has any role inappropriate ventilation (too low pCO2) I.e. mixed Alkalosis)?

Excellent discussion. While I may not fully agree with all below copy and pasted author statements, I included for fairness. If you only read one resource, I suggest the chapters from Complications of Dialysis edited by Norbert Lameire, Ravindra Mehta. While some of these are dated, the principles and simplified discussions are right on point and have stood the test of time.

Maintain as near physiologic normalcy in dialysis. Longer sessions coupled with more frequent treatments are generally tolerated better than load the boot shock and awe routines.

In 3 clinics, all patients on citric acid for 2+ years with 2.4 mEq/L--all with same dialysis fluid with same 35 bicarbonate concentration and oral bicarbonate as needed. excellent tolerance and performance. We have converted to a standard default of K+ 2.5, mag 1.3, Ca++ 2.25 due to lower serum K+ with more effective clearance due to increased time and more steady state bicarbonate levels. We've liberalized K+ diets. IDWG has not been of concern as thought with oral bicarbonate due to our standard default 135 sodium setting. No sodium variance profiling.

Symptomatology has improved (despite dialysis fluid sodium level) with lowering of UFR max and lower temperature setting with dialysis fluid to default of 35. Beware of large ultrafiltration rate and total volume Rx therapies and the unpredictability of alkali equivalent tolerance and chasing the dog's tail..bicarbonate space can be dynamic even in same patient with pH changes, water VoD changes and other physiologic factors.

Ca++ lowering effect with this low level of citric acid is minimal and only transient...however, if too high a delivery of bicarbonate and alkali equivalence is coupled with low Ca++ level, low Mag, low K, (whatever reason), clinical picture of alkalosis/hypocalcemia and other electrolyte imbalance may result. The resulting alkalosis issues can actually mimic intravascular volume compromise and lead to problems with accurate dry weight management.

lots of variables for predicting response: we simplified the prescription and went low and slow with ultrafiltration, BFR, UFR, DFR and time.

It is true that a good kinetic modeled prescribing nomogram would be nice...however, many errors occur in executing prescriptions that do not reflect what is intended by prescriber. The properties of the devices, equipment and the concentration gradient cannot do it alone: Time (duration of tx and time between tx), space (reaching and leaching), and patient factors are important.

We took those realities into consideration.

_____________________

“The optimal dialysate bicarbonate concentration is one that prevents acidosis at the beginning of the next haemodialysis session while avoiding postdialysis alkalosis.”

Dialysis A step towards optimal dialysate bicarbonate concentration

Basile, C. & Lomonte, C. Nat. Rev. Nephrol. 9, 565-566 (2013)

“Given this feedback loop between acid production and alkali addition and the fairly uniform nature of the dialysis prescription, two questions emerge: (1) Why does the serum bicarbonate concentration vary so widely from patient to patient? (2) Why can’t we easily devise a hemodialysis prescription that will normalize serum in all our patients?”

Acid-Base Homeostasis in End-Stage Renal Disease F. John Gennari Review Article Seminars in Dialysis 1996 Vol 9. No 5 (Sep-Oct)

“It is clear from this and other studies that optimal correction of acidosis is an essential component of adequacy of dialysis. How can this be achieved in dialysis?” Kenneth Graham et al JASN April 1, 1997 vol. 8 no.4 627-631

“The bicarbonate concentrations now used clinically were not derived from kinetic studies but came mostly from empirical evaluations of their clinical adequacy. However, since the individual requirement of buffer administration varies among patients, it is difficult to propose a universally adequate fixed concentration; the personalization of the dialysis bath would be useful in answering the individual needs.”

40: Organ and Metabolic Complications: Acid-Base pg 1021

Mariano Feriani, Claudio Ronco, Aldo Fabris and Giuseppe La Greca

Bench-to-bedside review: A brief history of clinical acid-base

David A Story

April 30, 2004

Approach to the Hemodialysis Patient with an Abnormal Serum Bicarbonate Concentration

Lisawat P, Gennari FJ Am J Kidney Dis 2014

Acid-Base balance in dialysis patients

Kidney International, Vol. 28 (1985), pp. 678-688

Principal Discussant: F. John Gennari

Leunissen KML, Kooman JP, Waterval PW, Claessons PJM, Van Hoof JP: Individualization of the dialysate bicarbonate concentration for optimal correction of acidosis. Blood Purification in Perspective: New Insights and Future Trends, Vol. II, edited by Mann NK, Botella J, Zucchelli P, Cleveland, ICAOT Press, 1992, pp 177-181

Clinical review: Reunification of acid-base physiology

John A Kellum

Crit Care. 2005; 9 (5): 500-507

Dilution acidosis and contraction alkalosis: Review of a concept

Kidney International Vol. 8, (1975), p. 279-283

Editorial Review

The concept of bicarbonate distribution space: The crucial role of body buffers

Kidney International, Vol. 36 (1989), pp. 747-752

Editorial Review

Oral Base Replacement in Patients on Hemodialysis

John C. Van Stone, M.D.

Ann Intern Med. 1984; 101 (2): 199-201

Severity of Metabolic Acidosis as a Determinant of Bicarbonate Requirements

Serafino Garella, M.D., Clare L. Dana, M.D., and Joseph A. Chazan, M.D.

N Engl J Med 1973; 289: 121-1126 July 19, 1973

Vol. 289 No. 3 Bicarbonate Therapy of Profound Acidosis—Garella ET AL pg 121

Correction of Acidosis in Hemodialysis Patients Increases the Sensitivity of the Parathyroid Glands to Calcium

Kenneth A. Graham, et al

Proc Clin Dial Transplant Forum. 1978 Nov 18-20;8:137-41.

Mass balance of base equivalents during hemodialysis: importance of organic acid anions.

Assomull V, Vreman HJ, Weiner MW.

Ann Intern Med. 1969 Dec;71(6):1105-11.

Acid-base status during the interdialytic period in patients maintained with chronic hemodialysis.

Acid-Base Homeostasis in End-Stage Renal Disease F. John Gennari Review Article Seminars in Dialysis 1996 Vol 9. No 5 (Sep-Oct)

Acetate Metabolism in Normal Human Subjects*

R. Henry Richards, M.D., Hendrik J. Vreman, Ph.D., Philip Zager, M.D., Charles Feldman, M.D., Terrance Blasche, M.D., and Michael W. Weiner, M.D.

Pg 1029 40: Organ and Metabolic Complications: Acid-Base

Replacement of Renal Function by Dialysis edited by Claude Jacobs

Acid-Base Hemodialysis pg 363-370 Gennari and Feriani

Complications of Dialysis edited by Norbert Lameire, Ravindra Mehta

Hakim rM, Pontzer M, Tilton D, Lazarus JM, Gottlieb MN. Effects of acetate and bicarbonate dialysate in stable chronic dialysis patients. Kidney Int 1985; 28: 535-540.

To Paul: You're a swollen river !!! Thirthy years of research in few minutes. Excellent for me. I upvote your answer and I' ll be your follower. However I would like to read "Approach to the Hemodialysis Patient with an Abnormal Serum Bicarbonate Concentration by Lisawat P, Gennari FJ Am J Kidney Dis 2014". Can you attach the paper?

To Jan: I have attached only one paper for you

Thank you Marco for the paper. I attached the fulltext you requsted.

It is misunderstanding, I calculated just like you, “triple load” meant in acid concentrate, 9 (from citrate) : 3 (from acetate). However, in my opinion the difference of 6 mmol/L could be critical in short posttreatement period. There is no difference in the total buffer base content of final dialysate, but in case of citrate the serum bicarbonate increase should be higher after finishing dialysis (compared to acetate). Do you agree?

Thank you, dr. Miller, for your experiences.

I can´t believe the excellent tolerance of your patients using citric acid with Ca++ 2.25. We have used Ca++ 2.5, bicarbonate 30-32, K+ 3, Mg++ 1, Na+ 138-140 (HDF, post- or predilution, QB 350-400, QD 700-800) and after 2 months we had to change to Ca++ 3 mEq/L in all patients. Later we had to finished citrate dialysis in half of patients, because of an increase of dry weight (1-4 kg/3 months), increase of parathormone by 200-400 pg/ml, hypotension, seizures. These complications have occurred even in patients with low UFR.

What´s wrong???

We measured calcium, magnesium and sodium mass balance during hemodialysis (not HDF) using continuous partial waste dialysate collection samples and we compared dialysis solution with citric and acetic acid using Ca++ 3 mEq/L. All balances were more negative in citrate solution: total Ca balance -58 vs. +180 mg, Mg balance -90 vs. +15 mg and Na balance -205 vs. +40.

We have considered these results to be the cause of complications.

to Jan. I agree: postdialysis bicarbonate increases more with citrate than with acetate.

Many thanks for the paper (another milestone paper from John Gennari!).

Quite stimulating discussion. My wasted years and current bench limitations require me to brush up to keep up with you guys.

Forgive my inability to upload some articles from my antiquated device program.

Jan (please call me Paul): there was a Korean researcher presentation I believe 2010 or 2011 regarding acetate and citric acid based concentrates that revealed bicarbonate yielding distribution curves over time during and post dialysis. It was a slide show presentation available on the web. I’ve been searching for it unsuccessfully.

It has been reported that age is a factor in delayed peak of acetate and I believe post dialysis. I may be incorrect, however, 2 hours comes to mind. I believe Ray Hakim’s study discussed this.

I’m searching for reasons why the tolerance to citrate is different for your patients.

So many potential variables (I’m thinking aloud and not necessarily for a response): could the higher efficiency of your HDF and DFR result in more rapid removal of active solutes? This has been reported. We feed our patients during dialysis with high biological value protein and amino acids?

Do you use standard Oxygen therapy during dialysis?

Have you tried administering oral calcium at beginning of dialysis for any of these patients to see if any prevention occurs with the symptoms?

Does the acetate metabolism counter some of the alkalosis effects?

Did they routinely experience nervousness, hyper-excitability and typical tingling and needles and pins sensations perioral and distal limbs after 2-3 hours of therapy?

Were the labs post treatment and during these symptoms suggestive of alkalosis and electrolyte imbalances?

Just curious: How much net gain exposure to sodium and chloride do your patients experience per week during therapy?

Are there any noticeable differences in those patients who develop these symptoms and those who have better tolerance? (muscle mass, nutrition, vintage on dialysis, age, vascular disease, laboratory baseline results, TBW, RBC volume, bone activity, etc)?

Marco: excellent comments in February under a different category. I do not have a good answer for you that you haven’t already covered in another forum. Maybe Uribarri does? He has posted good comments under a different, albeit, related topic as I recall.

Expanding upon the original question: I’m curious as to what you guys think about dialysis fluids that use lower sodium, lower chloride, and back to the slightly higher dextrose?

*I did not make the ERA-EDTA Amsterdam meeting. I did notice some interesting discussions regarding acidosis and sodium.

humble regards,

paul

_____________

J Crit Care. 2006 Dec;21(4):333-8.

Impact of chloride balance in acidosis control: the Stewart approach in hemodialysis critically ill patients.

Libório AB1, da Silva Alexandre C, Noritomi DT, Andrade L, Seguro AC

Braz J Med Biol Res, October 2010, Volume 43 (10) 996-1000

Effect of chloride dialysate concentration on metabolic acidosis in maintenance hemodialysis patients

F.O. Marques, A.B. Liborio, and E.F. Daher

Chloride, but not unmeasured anions, is correlated with renal bone disease markers

Alexandro Braga Liborio, Danilo Teixeira Noritomi, Manuel Carlos Martins de Castro

JNephrology 2007; 20: 000-000

www.sin-italy.org/jnonline- www.jnephrol.com

Dual-Concentrate Bicarboanate-Based Hemodialysis: Know Your Buffers

Orly F. Kohn, MD, Carl M. Kjellstrand MD and Todd S. Ing MD

August 24 2012 Original article published

Artificial Organs Volume 36, Issue 9, pages 765-768 September 2012

To paul Miller: thank you for your praise and suggestion. I'm looking for Uribarri

Acetate versus Citrate

The 12th annual congress of nephrology

Korea- Japan HDF Forum

Clinical Experience of Acetate-Free Citrate Dialysate

Sung Bae Park, M.D.

Department of Internal Medicine

Keimung University School of Medicine, Deagu, Korea

Chapter 10

Distubances in Acid-Base Balance in Patients on Hemodialysis

Alexandre Braga Liborio and Tacyano Tavares Leite

http://cdn.intechopen.com/pdfs-wm/43030.pdf

To Paul

first of all thanks again for your appreciation. Than thanks for " guys": I'm 50 y.o..

I've already read most of the abovementioned papers. Unfortunately Stewart has not yet arrived in Italy (at least in italian hemodialysis units) so that Cl- is yet the forgotten electrolyte, not the queen ones. As regard dialysis fluid only few years ago I've discovered it's more acid then patients' blood. I discovered its high CO2 tension and my studies are focused on these topics. As regard "my" dialysis fluid I usually prescribe Na 136-142 K 3 (rarely less than 3 for arrhithmya) Ca 1,5 HCO3 30 (35 in patients with high body weight) Acetate 3 Glucose 100 (rarely 0 because I've observed a lot of hypoglicemic crisis) but I also prescribe high KT/V (blood flow rarely less than 400 ml/min, times 240 min, Filter surface 1,5-2,1 m2) ad UF rate rarely above 800 ml/h. As regard Acetate I'm exstensively studing Acetate-Free Dialysate for lower CO2 tension than Bicarbonate dialysis.

My first love is diagnosis of acid base derangment (especially mixed ones) in hemodialysis patients

Hear Jan Havlin and you on these issues it will be a pleasure for me

Paul, I very much appreciate the debate concerning the citrate dialysate. It is very important to me, because six months ago hundreds of dialysed patients in the Czech Rep. started using this solution and many of them have difficulties.

To your questions:

They usually describe cramps in the distal lower limb after 2-3 hours of therapy and/or during the night after HDF, weakness after HDF. We noticed higher frequency of symptomatic hypotension after 2-3 hours of therapy. And all the symptoms were worsening (this is the reason why we suppose that it is related to intradialytic ion mass balances - loss of sodium?? calcium?? magnesium??). No typical tingling and needles and pins sensations perioral. Our reaction was increase of dry weight and increase of dialysate sodium and calcium. After few weeks we noticed that the symptoms were worsed and we started to return them back the original solution. Currently, only 20-25% of patients still used citrate solution in our dialysis center.

Noticable differences?: no obvoius differences, but we are trying to analyze it better.

My questions:

1) When you wrote about your experiences with citrate, it was HDF or HD? What is your dialysate flow rate?

2) Do you really use dialysate calcium 2.25? (in mmol/L is to low, in mEq/L is too high)?

3) What does exactly mean “feeding patients during dialysis with high biological value protein and amino acids”?

4) What is “standard Oxygen therapy during dialysis”?

5) We have never tried administering oral calcium at the beginning of dialysis? You are used to do that?

To Stewart:

Marco, I think that Italy can easily live without Stewart :)

Stewart’s critics (especially Ira Kurtz and Jeffrey Kraut - in my opinion the greatest experts for acid-base disorder - highly recommended “Kurtz I, Kraut J, Ornekian V, et al. Acid-base analysis: a critique of the Stewart and bicarbonate-centered approaches. Am J Physiol Renal Physiol 2008”, fulltext attached) consider his theory to be a mathematical construct not corresponding to causality. Its mechanistic interpretation, based on dependent and independent variables, is not supported by any evidence and there is even no theoretical model explaining how the change of strong ion concentration can affect pH. I agree that the Stewart model does not clarify the causality of acid-base disorder. Moreover, we cannot talk about the concept of dependent and independent variables in dialysis patients as we supply high amount of the independent variable bicarbonate three times a week.

But it's brilliant theory which is essentially irrefutable.

As written by Kurtz et al. (page 9) “In vitro, our experimentalist considers performing ion beam experiments, where an aqueous solution is bombarded with a charged ion beam, e.g., an Na ion beam, or a proton beam. In regard to the Na ion beam experiment, the Stewart model would predict that the addition of Na per se by increasing [SID] would increase the [H+]. The traditional acid-base would point out that adding Na+ would not result in a significant change in [H+] (other than a minor effect on Kw due to a change in ionic strength, and a minor shift in the equilibrium reaction because Na+ can combine to a small extent with OH-). The proton beam experiment is an example of H+ flux into an aqueous solution from a source external to the system that according to the Stewart formulation cannot alter the [H+] ; an argument based on epistemological considerations. The traditional acid-base physiologist would predict that the [H+] will indeed increase because of the change in the mass balance of H+”.

On the other hand Stewart concept and traditional approach do not contradict one another, but complement each other. Stewart’s analysis explicitly refers to a link of metabolic acid-base disorders with all plasma ions. Ion imbalances, primary or secondary, may help in specifying the cause of metabolic disorders. A fundamental difference between both analyses is the assessment of the relationship between sodium, chloride and bicarbonate. If both ions are still within the reference range, but, for example, plasma sodium is at the lower limit and/or plasma chloride at the upper limit (both ions have a very wide reference range), usually we do not consider its association with MAC, but the sodium-chloride difference is already significantly decreased.

To Marques and Liborio: I know these studies, I´m just preparing an article related to “acid-base disorder in patients on HDF”, where I am trying to comment them. I paste the relevant paragraphs:

To Marques:

Marques et al. argued that reducing the dialysate chloride concentration (by modifying sodium dialysate in the same proportion) will influence MAC due to the decrease of UA (retained unmeasured acid anions). This decline was explained by an increase of intracellular buffering capacity during the interdialytic period due to the lower intracellular chloride concentration on the basis of the Gibbs-Donnan effect. As an alternative hypothesis Marques pointed out the potential effect of lower dialysate chloride concentration on a higher clearance of strong acid anions, again based on the Gibbs-Donnan equilibrium.

However, when we divided the patients (our group of 68 patients on post-dilution HDF) into two groups according to the postdialysis chloride concentration, we found that in the high-chloride group (Cl- > 100 mmol/L, n = 38) the mean concentration of UA- was 0.2 mmol/L, whereas in the low-chloride group (Cl- < 101 mmol/L, n = 30) it was 4.4 mmol/L after dialysis. Furthermore, there was an absence of a significant correlation between intradialytic change of SBE (ΔSBE) and intradialytic change of Cl- (ΔCl). In accordance with other studies ΔSBE correlated only with ΔUA-. Based on these results, it seems that chlorides are likely to be increased in order to maintain plasma electroneutrality. This hypothesis is supported by the result in the distribution of file according to postdialysis concentration of UA-. After dialysis in the low-UA group (UA- < 2.3 mmol/L, n = 35) was significantly higher chloride concentration (101.1 vs 99.1 mmol/L), as well as bicarbonate (29.4 vs 27.1 mmol/L) and SBE (5.3 vs 2.6 mmol/L).

To Liborio:

Liborio described a similar phenomenon in dialysis patients with ARF, when a group of patients with higher predialysis chloride concentration - compared with dialysate concentration - had higher increase of SBE compared with the low-chlorides group, using the same hemodialysis parameters. First, it is a mistake to suppose that the same concentration of plasma and dialysate corresponds to neutral gradient (as already mentioned above in the discussion). Dialysate chloride concentration 109,5 mEq/L, in the case of standard protein concentration, leads after taking into account the Donnan coefficient of 0.96 to the reduction of plasma water chloride concentrations into 105 mEq/L. And after the conversion of plasma water on the plasma concentration the final chloride concentration is 97.8 mEq/L. It is ilustrated by decrease of Cl- from 108 to 107 mEq/L although we were expecting the chloride increase. The decrease from 108 to 107 mEq/L is quite low probably due to the hypoproteinemia in patients with ARF. Further, given that predialysis SBE were comparable in both groups, it is clear, that in low-chloride group had to be higher concentration of UA- (unfortunately authors did not publish these parameters for each group).

One can hypothesize, that the reason why the high-chloride group had higher SBE is the combination of hyperchloremic acidosis and acidosis with higher AG, where, unlike the second group, correction runs parallel in two ways: by elimination of UA- and by substitution of missing bicarbonate, while SBE of low-chloride group depends especially on the quantity of eliminated UA-. Given that results we can conclude that combinated MAC is easier correctable by dialysis than simple MAC with increased AG. This theory is supported by our results: after splitting the file into two groups according to predialysis chloride concentration, low-chloride group (Cl 103, n = 29). In both groups were predialysis SBE comparable, but differed in UA-, which was higher in low-chloride group. Postdialysis SBE was significantly higher in high-chloride group, ie the group with predialysis lower concentration of UA-. In both groups was UA- decrease comparable.

I hope you will share your paper as soon as published. Now I thanks you for sharing here part of the results. Good luck for the paper

to Paul:

It seems that the difference between patients using citrate dialysate who developed symptoms and those who had better tolerance is the bone activity and active vitamin D supplements. The patients with better tolerance had low PTH or higher doses of calcitriol.

What is the PTH level and calcitriol, paricalcitol and cinacalcet dosage of your patients?

Dear All,

have you read  "Higher serum bicarbonate in dialysis patients is protective", Pro Con and Moderator's point of view just published on NDT?

https://ndt.oxfordjournals.org/content/current

Dear colleagues

I have some answers to our old questions. After working last years with F John Gennari and with John Sargent I am able to understand what are determinants of serum bicarbonate concentration during standard hemodialysis treatment. With not a little surprise now I can state that acetate contribution to alkalinization is close to 35% despite its low bath concentration; I have to acknowledge the meaningful role of ultrafiltration on acid-base issue and finally I learned that new organic acid production is a side effect of base addition. There is a lot for a new discussion

Marco

Article Acid‐base homeostasis during hemodialysis: New insights into...