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4.5 Dialysate (Guidelines 5.1 – 5.4)

4.5 Dialysate (Guidelines 5.1 – 5.4)

When the 2nd edition of the RA Guidelines was published in 1997, the only recommendation relating to the composition of the dialysate was that renal units phase out the use of acetate in favour of bicarbonate buffering, since the improved efficiency of dialysis could overwhelm the capacity to metabolise acetate. The need to keep bicarbonate separate from divalent cations to prevent precipitation meant that dialysate had to be produced using two different concentrates, leading to the modern proportioning system in which sodium bicarbonate is mixed with an electrolyte concentrate (‘acid concentrate’) at the point of use, allowing independent control of most dialysate constituents. Some dialysate constituents have diversified whereas others have gradually become standardized. Dialysate calcium was often supra physiological in the 1990’s (around 1.75mmol/L) to prevent hypocalcaemia, but this became unnecessary with increasing use of vitamin D analogues and calcium containing phosphate binders, so that dialysate calcium has become reasonably standardized, usually in the range 1.25 1.50mmol/L. Non standard dialysate calcium may sometimes be helpful, for example in the context of calciphylaxis, but this is usually driven by bone mineral considerations and is outside the scope of this guideline. In the 1990’s, dialysate was usually glucose free due to cost and microbiological concerns, and hypoglycaemia was often a problem for diabetic patients. Glucose containing dialysate was initially prescribed for diabetic patients, but extended to all as costs improved, so that a dialysate glucose of 5.5mmol/L is now standard in almost all UK dialysis units. The other constituent of dialysis that has become standardised is magnesium, with low (usually 0.25 or 0.375mmol/L) or high (usually 0.75mmol/L) magnesium being replaced by a dialysate magnesium of 0.5mmol/L, close to the lower end of the normal range. Opposing these trends, there has been significant diversification in dialysate potassium, and similarly, buffer concentrations and practices vary between units and manufacturers, and are discussed below.

Guideline 5.1 Selection of dialysate potassium

We recommend an optimal pre dialysis serum potassium in the range 4.0–6.0mmol/L, remembering to consider measurement errors (e.g., due to haemolysis) when interpreting levels. [1B]

We suggest choosing dialysate potassium between 1.0 and 3.0mmol/L for the majority of patients, using an individualised approach, in general using the highest dialysate potassium that is sufficient to control pre dialysis hyperkalaemia. [2C]

We suggest a combined approach to managing hyperkalaemia, which may include decreasing dialysate potassium and/or other measures, including dietary advice, medication review and increased dialysis frequency. [2D]

Rationale

Historically, it was often difficult to remove the potassium accumulated between dialysis sessions, so dialysate potassium between zero and 2mmol/L was common. The requirement for dialysate with potassium levels that are close to, or within, the normal range reflects the increased efficiency of modern dialysis and the increased age of the modern patient. In most units dialysate potassium is determined by the choice of acid concentrate: zero potassium is no longer used, and suppliers offer concentrates with potassium between 1 and 4mmol/L.

Removal of accumulated potassium by intermittent haemodialysis inevitably leads to a fluctuating profile of serum potassium with a risk of cardiac arrhythmias at both high and low concentrations. This probably contributes to the clustering of sudden cardiac death around the peridialytic period, and at the end of the weekend gap [1].

Both low and high pre dialysis potassium are associated with increased mortality, so that the mortality curve is U shaped. Low potassium often appears more harmful in unadjusted data: for example, in a study of 483 Taiwanese patients followed from 2004 to 2008, Hwang showed that those with pre dialysis potassium below 3.5mmol/L had more than twice the risk of mortality than those with higher levels [2]. But this link may be due to confounding by comorbidity malnutrition: in a much larger study of 74,219 patients between 2001 and 2004, a U shaped risk curve was seen, with increased mortality with pre dialysis potassium outside the range 4.3–5.6mmol/L [3]. After adjustment for case mix and malnutrition parameters however, the increased risk of mortality remained only for the high potassium patients (though the less than 4.0mmol/L category was not subdivided). The optimum pre dialysis potassium therefore appears to be above 4.0 with an upper limit between 5.6 and 6.0mmol/L, though the broader range seems more appropriate given the considerations below.

The relationship between post dialysis potassium and mortality is unknown, as it is rarely measured, but the risks of post dialysis hypokalaemia can be inferred from studies of dialysate potassium [4,5]. For example, Pun compared 502 patients who experienced sudden cardiac arrest in dialysis units between 2002 and 2004, with 1632 age and vintage matched controls, finding that risk was doubled if the patient last dialysed with a low dialysate potassium (less than 2.0mmol/L) [4].

The DOPPS review of modifiable practices associated with sudden death included 36,235 patients in 12 countries of whom 6606 were dialysed with dialysate potassium at least 3.0mmol/L [6]. An increased risk of sudden death was observed with dialysate potassium below 3.0mmol/L (HR 1.17, 95%CI 1.01–1.37), though it was not clear if this risk extended to those with pre dialysis serum potassium over 5.0mmol/L. Others have suggested that lower dialysate potassium may prevent sudden death in this subgroup [1,3], but the latest DOPPS analysis found no meaningful difference in mortality or arrhythmia events between patients treated with dialysate potassium of 2.0 or 3.0mmol/L [7].

The understandably strong impulse to control pre dialysis hyperkalaemia should therefore be tempered by consideration of the less visible risk of post dialysis hypokalaemia. Pragmatically therefore one can conclude the following general principles:

  • Firstly, pre dialysis hyperkalaemia should be controlled, though an overly tight range may be counterproductive, so the previously recommended target for pre dialysis potassium still seems optimal (4.0 – 6.0mmol/L). Caveats to interpreting this range should be noted: firstly, achievement of pre dialysis potassium within this range does not necessarily mean that dialysate potassium is optimal, and secondly, consistent adherence to treatment is most likely just as important as specifics of the potassium range or dialysis prescription.
  • Secondly, non dialysate approaches to hyperkalaemia may sometimes be more favourable [8,9]. Dietary reduction may be preferable if it can be achieved without an adverse effect on protein calorie intake, and other dialysis changes may be appropriate, such as increasing blood flow, duration or frequency. Consideration could also be given to potassium binding resins [10].
  • Thirdly, lower dialysate potassium does increase the removal of potassium during each session [11], and based on the risk of arrhythmias due to hyperkalaemia, dialysate potassium should be reduced if other measures are not possible or successful [12]. However, dialysate potassium should be no lower than is necessary to achieve this goal – individualization does therefore seem necessary, so that each patient uses the highest dialysate potassium which still controls pre dialysis hyperkalaemia. This pragmatic approach has probably driven the steady increase in the use of higher potassium dialysates, and reduction in the use of concentrations below 2.0mmol/L, over the 5 DOPPS phases between 1996 and 2015 [7].
  • Finally, and particularly for measurements taken remote from the laboratory, the relatively high frequency of measurement errors (for example due to in vitro haemolysis) should be remembered when interpreting potassium levels.

References

  1. Huang CW, Lee MJ, Lee PT, et al., Low Potassium Dialysate as a Protective Factor of Sudden Cardiac Death in Haemodialysis Patients with Hyperkalemia. PLoS One. 2015 Oct 6;10(10): e0139886.
  2. Hwang JC, Wang CT, Chen CA, et al., Hypokalemia is associated with increased mortality rate in chronic haemodialysis patients. Blood Purif. 2011;32(4):254 61.
  3. Kovesdy CP, Regidor DL, Mehrotra R, et al., Serum and dialysate potassium concentrations and survival in haemodialysis patients. Clin J Am Soc Nephrol. 2007 Sep;2(5):999 1007.
  4. Pun PH, Lehrich RW, Honeycutt EF, et al., Modifiable risk factors associated with sudden cardiac arrest within haemodialysis clinics. Kidney Int. 2011 Jan;79(2):218 27.
  5. Karnik JA, Young BS, Lew NL, et al., Cardiac arrest and sudden death in dialysis units. Kidney Int. 2001 Jul;60(1):350 7.
  6. Jadoul M, Thumma J, Fuller DS, et al., Modifiable practices associated with sudden death among haemodialysis patients in the Dialysis Outcomes and Practice Patterns Study. Clin J Am Soc Nephrol. 2012 May;7(5):765 74.
  7. Karaboyas A, Zee J, Brunelli SM, et al., Dialysate Potassium, Serum Potassium, Mortality, and Arrhythmia Events in Haemodialysis: Results From the Dialysis Outcomes and Practice Patterns Study (DOPPS). Am J Kidney Dis. 2017 Feb;69(2):266 277.
  8. Gutzwiller JP, Schneditz D, Huber AR, et al., Increasing blood flow increases Kt/V(urea) and potassium removal but fails to improve phosphate removal. Clin Nephrol. 2003 Feb;59(2):130 6.
  9. Tucker B, Moledina DG. We Use Dialysate Potassium Levels That Are Too Low in Haemodialysis. Semin Dial. 2016 Jul;29(4):300 2.
  10. Noureddine L, Dixon BS., Complications and management of hyperkalemia: implications for the use of the novel cation exchangers zirconium cyclosilicate and patiromer. Clin. Invest. (Lond). 2015;5(10): 805–23.
  11. Agar BU, Culleton BF, Fluck R, et al., Potassium kinetics during haemodialysis. Hemodial Int. 2015 Jan;19(1):23 32.
  12. Di Iorio B, Torraca S, Piscopo C, et al., Dialysate bath and QTc interval in patients on chronic maintenance haemodialysis: pilot study of single dialysis effects. J Nephrol. 2012 Sep Oct;25(5):653 60.

Guideline 5.2 Selection of dialysate buffer

We recommend an optimal pre dialysis serum bicarbonate in the range 18.0 26.0mmol/L, remembering to consider measurement errors (e.g., due to exposure to air) when interpreting levels. [1C]

We suggest the term ‘dialysate buffer’ rather than ‘dialysate bicarbonate’ to avoid confusion arising from differences in manufacturers’ terminology. [2C]

We suggest choosing dialysate buffer below or equal to 37.0mEq/L for the majority of patients, using a standardised or individualised approach. [2C]

We suggest a combined approach to abnormal pre dialysis serum bicarbonate, which may include increasing dialysis dose, oral bicarbonate, nutritional support, or individualising dialysate buffer. [2D]

Rationale

The literature on dialysate bicarbonate is difficult to interpret due to unclear definitions when reporting the bicarbonate and additional alkali components. Most commonly, the electrolyte concentrate contains a non bicarbonate acid, to reduce the deposition of calcium and magnesium salts – acetic acid is perhaps the most common, but citric acid and sodium diacetate may also be used.

When mixed to form the dialysate, acetate reacts with sodium bicarbonate to form sodium acetate, water, and carbon dioxide:

HC2H3O2 + NaHCO3 → NaC2H3O2 + H2O + CO2

The addition of 3mmol of acetic acid to a litre solution containing 35mmol of bicarbonate therefore reduces the bicarbonate concentration to 32mmol/L. In publications, bicarbonate concentration in this dialysate may variably be referred to as having a bicarbonate concentration of 32 or 35mmol/L, with the acetate content rarely reported.

In addition, the bicarbonate ‘setting’ on machines from different manufacturers refers variably to the bicarbonate concentration either prior to (e.g., Braun) or after (e.g., Fresenius) mixing with the electrolyte concentrate. The terms ‘actual’ bicarbonate (because that is what is actually added as sodium bicarbonate) and ‘final’ bicarbonate (because that is the bicarbonate in the dialysate at the point of use) are sometimes used to separate their meaning. However, the total buffer concentration remains the same before and after this mixing, so this term has a clear unambiguous meaning (equivalent to the sum of bicarbonate and acetate concentrations in the final dialysate). In a discussion of the DOPPS study of dialysate bicarbonate, Tentori observed that when asked either for the bicarbonate or total buffer concentration, most DOPPS units returned the same figure, suggesting that clinicians generally mean ‘actual’ rather than ‘final’ bicarbonate, which is the same as total dialysate buffer [1 3].

The factors affecting pre dialysis serum bicarbonate levels include protein intake, residual kidney function, interdialytic fluid gain, dialysate buffer concentration, dialysis adequacy, oral sodium bicarbonate, and other alkaline medications such as calcium carbonate [4].

Observational studies of pre dialysis levels usually show a J shaped mortality curve, with most of the excess risk associated with high levels of bicarbonate [5,6], but this appears to be due to the close link between high bicarbonate and malnutrition. For example, in a study of 56,385 patients between 2001 and 2003, Wu observed a progressive increase in mortality as pre dialysis bicarbonate increased beyond 23mmol/L, but also strong associations between higher bicarbonate and worsening markers of nutrition including albumin, phosphate, and protein intake [7]. When adjusted for comorbidity and 12 parameters associated with malnutrition, most of the increased mortality appears with low bicarbonate, at levels below 18–21mmol/L. Some guideline groups have therefore increased the lower limit for optimal pre dialysis bicarbonate to 20 or 22mmol/L [8,9].

Post dialysis bicarbonate is rarely measured, but three considerations argue for caution in attempting to achieve a minimum pre dialysis bicarbonate. Firstly, the risks associated with abnormal bicarbonate are less clear and of a lower magnitude than those associated with abnormal potassium (mortality hazard ratio of approximately 1.2 for the most extreme category of bicarbonate versus 1.5 for potassium).

Secondly, although it is principally low bicarbonate which carries risk, high pre dialysis bicarbonate also appears to be harmful. Whilst much of the risk observed is attenuated by adjustment, pre dialysis bicarbonate is still associated with increased mortality at levels above 27mmol/L [7]. Additionally, an increased risk of peri dialytic cardiac arrest has been observed with high pre dialysis bicarbonate: a Fresenius Medical Care memo in 2011 reported an internal case control study of 941 patients in 667 facilities who suffered cardiac arrest in 2010. Risk was 4.7 times higher in patients with pre dialysis bicarbonate over 28mmol/L, and 6.3 times higher if they also had pre dialysis potassium below 4mmol/L [10].

Thirdly, high dialysate buffer is associated with increased mortality. For example, in a large study of dialysate buffer using DOPPS data (collected from 17,031 dialysis patients in 11 countries between 2002 and 2011), Tentori observed a lower risk of mortality in patients treated with dialysate buffer less than or equal to 32mmol/L, regardless of pre dialysis bicarbonate (HR 0.90, 95%CI 0.80–1.01) and higher risk with dialysate buffer at or above 38mmol/L (HR 1.07, 95%CI 0.97–1.19) [1].

Pragmatically, therefore, one can conclude the following general principles:

Firstly, pre dialysis acidaemia should be controlled, though an overly tight range may be counterproductive, so the previously recommended lower target for pre dialysis bicarbonate still seems optimal, though the upper target could safely be increased (18.0–26.0mmol/L). As with potassium, achievement of this range does not necessarily ensure optimal dialysis prescription.

Secondly, dialysate buffer at or over 38mmol/L should generally be avoided, and the optimal dialysate buffer for the majority of patients is probably in the region of 32–35mmol/L.

Thirdly, many other factors affect pre dialysis bicarbonate, the dominant ones being nutritional state and dialysis dose, so that abnormalities of pre dialysis bicarbonate should not lead clinicians automatically to think of adjusting dialysate buffer. High bicarbonate in particular should prompt a nutritional thought process initially. It is not clear that adjustment of dialysate buffer is a helpful strategy for optimising pre dialysis bicarbonate, or that such an adjustment has much impact on pre dialysis bicarbonate levels. Specific groups however, such as patients with abnormal levels despite optimal diet and dialysis strategy, may have something to gain from dialysate buffer adjustment. Conversely, increased dialysate buffer may be more hazardous in certain circumstances, such as in combination with low potassium dialysate [11,12].

Whilst it is a very reasonable thing to do, and might prove to be beneficial in future studies, it is not currently clear that individualization of dialysate buffer is superior to standardization.

Finally, and particularly for measurements taken remote from the laboratory, the relatively high frequency of measurement errors (for example due to carbon dioxide escape) should be remembered when interpreting bicarbonate levels [13,14].

References

  1. Tentori F, Karaboyas A, Robinson BM, Morgenstern H, Zhang J, Sen A, Ikizler TA, Rayner H, Fissell RB, Vanholder R, Tomo T, Port FK. Association of dialysate bicarbonate concentration with mortality in the Dialysis Outcomes and Practice Patterns Study (DOPPS). Am J Kidney Dis. 2013 Oct;62(4):738 46.
  2. https://ajkdblog.org/2013/07/25/dialysis bicarbonate concentration do we know the right amount/
  3. Lew SQ, Kohn OF, Cheng YL, Kjellstrand CM, Ing TS. Three Stream, Bicarbonate Based Haemodialysis Solution Delivery System Revisited: With an Emphasis on Some Aspects of Acid Base Principles. Artif Organs. 2017 Jun;41(6):509 518.
  4. Kraut JA, Madias NE. Metabolic Acidosis of CKD: An Update. Am J Kidney Dis. 2016 Feb;67(2):307 17.
  5. Lowrie EG, Lew NL: Death risk in haemodialysis patients: The predictive value of commonly measured variables and an evaluation of death rate differences between facilities. Am J Kidney Dis 15: 458–482, 1990.
  6. Bommer J, Locatelli F, Satayathum S, Keen ML, Goodkin DA, Saito A, Akiba T, Port FK, Young EW. Association of predialysis serum bicarbonate levels with risk of mortality and hospitalization in the Dialysis Outcomes and Practice Patterns Study (DOPPS). Am J Kidney Dis. 2004 Oct;44:661 71.
  7. Wu DY, Shinaberger CS, Regidor DL, McAllister CJ, Kopple JD, Kalantar Zadeh K. Association between serum bicarbonate and death in haemodialysis patients: is it better to be acidotic or alkalotic? Clin J Am Soc Nephrol. 2006 Jan;1:70 8.
  8. EBPG Guideline on Nutrition 2007
  9. KDOQI Nutrition in Chronic Renal Failure 2000
  10. http://www.renalweb.com/writings/alkalosis/WithinFMC.htm
  11. Di Iorio B, Torraca S, Piscopo C, Sirico ML, Di Micco L, Pota A, Tartaglia D, Berardino L, Morrone LF, Russo D. Dialysate bath and QTc interval in patients on chronic maintenance haemodialysis: pilot study of single dialysis effects. J Nephrol. 2012 Sep Oct;25(5):653 60.
  12. Heguilén RM, Sciurano C, Bellusci AD, Fried P, Mittelman G, Rosa Diez G, Bernasconi AR. The faster potassium lowering effect of high dialysate bicarbonate concentrations in chronic haemodialysis patients. Nephrol Dial Transplant. 2005 Mar;20(3):591 7.
  13. http://www.mayomedicallaboratories.com/test catalog/Clinical+and+Interpretive/876
  14. Bandi ZL. Estimation, prevention, and quality control of carbon dioxide loss during aerobic sample processing. Clin Chem. 1981 Oct;27(10):1676 81.

Guideline 5.3 Supplementation of dialysate with phosphate

We suggest considering supplementation of the dialysate with phosphate in patients on augmented dialysis schedules. [2D]

Rationale

The conventional haemodialysis patient struggles to achieve sufficient phosphate removal, and historically dialysate has always been phosphate free. Guidelines usually focus more on the upper limit than the lower limit for optimal pre dialysis phosphate, and ranges in the region of 1.1 1.7mmol/L are often suggested, with most of the emphasis on treatments to reduce phosphate – indeed, most of the Renal Association’s advice on phosphate can be found in the guideline on mineral bone management. However, with demographic and treatment trends of the last decade, low phosphate is becoming more common, and since the symptoms of hypophosphataemia are non specific [1], this problem may be easily overlooked.

The relationship between pre dialysis phosphate and mortality is J shaped, with increased risk occurring at both high and low levels. But phosphate is strongly associated with age and nutritional state, so that the mortality risk associated with low phosphate is substantially (although incompletely) attenuated by adjustment for comorbidity and malnutrition [2]. In the context of low pre dialysis phosphate therefore, the main clinical focus should be on nutritional assessment and support.

When patients are unable to consume sufficient phosphate to match intradialytic loss, supplementation of the dialysate is a logical approach to managing hypophosphataemia. The argument for supplementation is generally accepted in the context of augmented dialysis, when post dialysis phosphate is often measured, and may be found to be very low in well nourished patients [3]. It is common practice, for example, to supplement dialysate with phosphate in pregnant patients receiving daily dialysis.

Supplementation could also be used to prevent undesired loss of phosphate in patients on conventional regimes with low pre dialysis phosphate that is refractory to other measures [4]. While this does appear to be clinically helpful in case reports, data to support this approach remain limited. However, as patients with low pre dialysis phosphate currently receive a form of dialysis which inevitably worsens this abnormality, so the instinct to ‘do no harm’ may be a sufficiently persuasive argument for some clinicians.

Phosphate precipitates in solutions containing calcium or magnesium, so like bicarbonate, must be added to the electrolyte concentrate at the point of use, but there is currently no commercially available phosphate additive approved for use in intermittent haemodialysis [5,6]. ‘In house’ supplementation can be achieved by adding phosphate salts to the electrolyte concentrate at the start of the session, but solutions intended for intravenous use typically contain potassium and are too dilute. Pharmaceutical grade phosphate salts in powder form can be used, but require quality assurance on storing, weighing, adding, and ensuring complete dissolution. The most common method is therefore ‘off label’ use of solutions intended as enemas: Cleen (formerly Fleet) Enema for example, is very suitable for enriching dialysate [7], although it contains antimicrobial preservatives (benzalkonium chloride and disodium edetate) which are widely used in medical products such as eye drops, which might have adverse effects in this context. The use of Cleen Enema in dialysate has a good safety record however: Pierratos first reported its use in nocturnal dialysis in the late 1990s [8], and frequent dialysis programmes in many countries have adopted this method [9,10]. Practical advice on adding phosphate to dialysate is provided in Appendix D.

References

  1. Brunelli SM, Goldfarb S. Hypophosphatemia: clinical consequences and management. J Am Soc Nephrol. 2007 Jul;18(7):1999 2003.
  2. Lertdumrongluk P, Rhee CM, Park J, Lau WL, Moradi H, Jing J, Molnar MZ, Brunelli SM, Nissenson AR, Kovesdy CP, Kalantar Zadeh K. Association of serum phosphorus concentration with mortality in elderly and nonelderly haemodialysis patients. J Ren Nutr. 2013 Nov;23(6):411 21.
  3. Hanudel MR, Froch L, Gales B, Jüppner H, Salusky IB. Fractures and Osteomalacia in a Patient Treated With Frequent Home Haemodialysis. Am J Kidney Dis. 2017 [Epub ahead of print]
  4. Ing TS, Chebrolu SB, Cheng YL, Yu AW, Choi P, Kjellstrand CM. Phosphorus enriched hemodialysates: formulations and clinical use. Hemodial Int. 2003 Apr 1;7(2):148 55.
  5. Sam R, Tang HL, Kjellstrand CM, Ing TS. Preventing/treating hypophosphatemia by adding phosphate to the dialysate. Int J Artif Organs. 2015 Dec;38(12):671 2.
  6. Godaly G, Carlsson O, Broman M. Phoxilium(®) reduces hypophosphataemia and magnesium supplementation during continuous renal replacement therapy. Clin Kidney J. 2016 Apr;9(2):205 10.
  7. Cleen Ready to Use 21.4g/9.4g Enema PIL (2013) www.medicines.org.uk/emc/PIL.20176.latest.pdf [last accessed August 2017]
  8. Pierratos A. Nocturnal home haemodialysis: an update on a 5 year experience. Nephrol Dial Transplant. 1999 Dec;14(12):2835 40.
  9. Su WS, Lekas P, Carlisle EJ, Cowin R, Bellamy J, Margetts PJ, Brimble KS, Clase CM, Gangji AS. Management of hypophosphatemia in nocturnal haemodialysis with phosphate containing enema: a technical study. Hemodial Int. 2011 Apr;15(2):219 25.
  10. Ebah LM, Akhtar M, Wilde I, Hookway G, Vincent M, Reeves C, Denton J, Woods J, Mitra S. Phosphate enrichment of dialysate for use in standard and extended haemodialysis. Blood Purif. 2012;34(1):28 33.

Guideline 5.4 Paediatric dialysate considerations

We recommend individualisation of dialysate electrolyte concentrations, including potassium, buffer, and calcium. [1C]

We suggest an individualised dialysate temperature, between core temperature and 0.5°C below, with monitoring of intradialytic core temperature for neonates and smaller children. [2D]

Rationale

Adult guidelines for dialysate composition (sections 5.1 – 5.3) are generally applicable to children, though there are a number of additional considerations.

In children with residual kidney function, tubular dysfunction is not uncommon, leading to electrolyte wasting and hypokalaemia or acidosis. Calcium balance is also more complex in children: the normal range for calcium is age dependent, and growing children require a positive calcium balance, so that hypocalcaemia may be both more common and more harmful, and yet vascular calcification is sometimes seen even in children and adolescents, in whom calcium phosphate product is an important risk factor [1,2]. Similarly, dietary protein intake is often proportionately greater than that of adults, and pre dialysis acidosis therefore more common.

The complexity and clinical heterogeneity of these issues therefore argues strongly for a more individualized approach to dialysate composition in children [3].

Thermal exchanges during dialysis may also be more significant, particularly in neonates and younger children, due to the proportionately greater blood flow, and sometimes a reduced capacity for compensation due to body size. Hypothermia should therefore be avoided by individualising dialysate temperature, with intradialytic monitoring in those most at risk. Control of thermal exchanges is available on some modern dialysis machines.

References

  1. Oh J, Wunsch R, Turzer M, Bahner M, Raggi P, Querfeld U, Mehls O, Schaefer F (2002) Advanced coronary and carotid arteriopathy in young adults with childhood onset chronic renal failure. Circulation 106:100–105.
  2. Goodman WG, Goldin J, Kuizon BD, Yoon C, Gales B, Sider D, Wang Y, Chung J, Emerick A, Greaser L, Elashoff RM, Salusky IB (2000) Coronary artery calcification in young adults with end stage renal disease who are undergoing dialysis. New Engl J Med 342:1478–1483.
  3. Fischbach M, Terzic J, Menouer S, Provot E, Bergere V (2001) Haemodialysis in children: principles and practice. Semin Nephrol 21:470–479.