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Medical Associates  ·  Department of Nephrology ← Maintenance Hemodialysis module  ·  urinenephrology.org
Clinical Mastery Series  ·  Maintenance Hemodialysis

Dialysate calcium, bicarbonate, magnesium, and glucose

The other active ingredients of the dialysate: guideline ranges, outcome signals, and how to choose within them
Andrew Bland, MD, FACP, FAAP UICOMP · UDPA · Butler COM Reviewed September 2026 17 min read

Bottom line

Part of the Maintenance Hemodialysis mastery module. Potassium and sodium have their own pages; this page covers the other active ingredients of the dialysate.

  • Calcium: stay between 2.5 and 3.0 mEq/L (1.25–1.50 mmol/L). KDIGO 2017 suggests this range (grade 2C) 1. Below 2.5 mEq/L is associated with sudden cardiac arrest, heart-failure admissions, and hypotension 2,3; 3.5 mEq/L is associated with calcium loading, faster coronary calcification, and higher mortality 4,5,6.
  • Buffer: the dose is the total buffer, not the number on the screen. Acetate or citrate in the acid concentrate adds to the bicarbonate setting 7,8,9. Higher dialysate bicarbonate was associated with higher mortality (HR 1.08 per 4 mEq/L) 10, and the UK guideline suggests a total buffer at or below 37 mEq/L for most patients 7.
  • A high pre-dialysis bicarbonate usually means poor protein intake, not too little alkali in the bath 7,11.
  • Magnesium: 1.0 mEq/L (0.5 mmol/L) is the standard, and it lowers plasma magnesium during most sessions 7,12. Higher serum magnesium is associated with lower cardiovascular and sudden death 13,14, but the outcome trial of a higher bath (Dial-Mag) has not reported 15.
  • Glucose: 100 mg/dL (5.6 mmol/L) is the standard. Glucose-free dialysate causes frequent silent hypoglycemia (NNT 5 to prevent one hypoglycemic patient per session) 16; 200 mg/dL adds hyperglycemia without further benefit 17; even with glucose in the bath, 21% of diabetic patients had unrecognized hypoglycemia on continuous glucose monitoring 18.
  • Divalent ions change their number when the unit changes. Always write the unit: a calcium bath of 2.5 mEq/L is 1.25 mmol/L.
ComponentmEq/Lmmol/Lmg/dL
Calcium 2.5 / 3.0 / 3.52.5 / 3.0 / 3.51.25 / 1.50 / 1.75—
Magnesium 1.0 / 1.51.0 / 1.50.5 / 0.751.2 / 1.8
Bicarbonate and acetateNumerically identical (monovalent)—
Glucose 100 / 200—5.6 / 11.1100 / 200

1. Dialysate calcium

Guideline position

KDIGO 2017 recommendation 4.1.4 suggests a dialysate calcium concentration between 1.25 and 1.50 mmol/L (2.5 and 3.0 mEq/L) in CKD G5D, grade 2C. The 2009 wording was kept; the grade was upgraded from 2D because of newer RCTs, which still could not separate 1.25 from 1.50 mmol/L 1. The 2023 KDIGO CKD-MBD Controversies Conference concluded that the 2017 recommendations remain largely consistent with the evidence 19, and UK practice has standardized in the same range 7. Phosphate and binder choice are covered in Phosphate management in ESRD.

Calcium balance and the case against a high bath

The 2009 assumption that 1.25 mmol/L yields neutral calcium balance was challenged by kinetic modeling: more than 500 mg of calcium can move in a single session, and an estimated 70% of patients on calcium-based binders (and 20%–50% on non-calcium binders) would need a dialysate below 2.5 mEq/L to avoid long-term accumulation 6. KDIGO acknowledges this challenge 1. Balance depends on the serum-dialysate gradient, ultrafiltration volume, and oral calcium and vitamin D exposure, which is why one dialysate calcium cannot be right for everyone.

  • Ok 2016 (RCT): 425 patients with intact PTH of 300 pg/mL or less randomized to 1.25 versus 1.75 mmol/L for 24 months. Coronary artery calcium progressed more slowly on 1.25 (P = .03), and biopsy-proven low bone turnover fell from 85.0% to 41.8% on 1.25 with no change on 1.75 5. Appraisal: surrogate endpoints, and the comparator was 1.75 mmol/L, not the 1.50 that many units consider “high.”
  • Kim 2015 (observational): in 1,182 incident Korean patients, 3.5 mEq/L was associated with higher mortality than 3.0 (HR 2.23, 1.28–3.90) and than 2.5–2.6 (HR 3.67, 1.78–7.55) 4.

The case against going too low

Study (design)Finding
Pun 2011 (case-control) 20502 in-clinic sudden cardiac arrests vs 1,632 matched controls: low-calcium dialysate among factors associated with arrest
Pun 2013 (case-control) 2510 witnessed arrests vs 1,560 controls: dialysate calcium below 2.5 mEq/L, OR 2.00 (1.40–2.90); larger serum-dialysate gradient OR 1.40 (1.10–1.80); greater intradialytic BP fall on low-calcium baths
Brunelli 2015 (facility cohort) 3Facilities converting from 2.5 mEq/L to lower defaults: heart-failure hospitalization RR 1.27 (1.06–1.51), hypocalcemia RR 1.39 (1.20–1.60), intradialytic hypotension RR 1.05 (1.01–1.10); no mortality difference; more binders, vitamin D, and calcimimetics used
MiD loop-recorder study 2019 (cohort) 2166 patients: dialysate calcium above 2.5 vs 2.5 mEq/L associated with fewer reviewer-confirmed arrhythmias (IRR 0.52, 0.39–0.70)
van der Sande 1998 (physiologic) 22NYHA III–IV patients: 1.25 vs 1.75 mmol/L lowered BP and stroke distance; ionized calcium drives contractility during ultrafiltration
Kyriazis 2004 (crossover) 23Dialysate calcium 1.25 with magnesium 0.25 mmol/L dropped mean arterial pressure by 15.2%, with falls in cardiac and stroke index

QTc. In a 23-patient crossover, 1.25 mmol/L lowered ionized calcium and lengthened QTc (403 to 419 ms) and QTc dispersion (38 to 49 ms), while 1.50 and 1.75 did not 24. In 330 incident patients, lower pre-dialysis ionized calcium was associated with a longer QTc (8.55 ms, 2.13–14.97), though dialysate calcium itself was not 25. KDIGO’s volume conference summarized the tension: higher dialysate calcium gives more hemodynamic stability and more calcium loading, and very low dialysate calcium should generally be avoided 26.

Calcimimetics

Cinacalcet and etelcalcetide lower serum calcium, which changes the serum-dialysate gradient without anyone touching the bath.

  • In EVOLVE (RCT, 3,883 patients), hypocalcemia within 16 weeks occurred in 58.3% on cinacalcet versus 14.9% on placebo (absolute increase 43.4%, NNH 3), and was severe (below 7.5 mg/dL) in 18.4% versus 4.4% (absolute increase 14.0%, NNH 8). Most episodes were asymptomatic and resolved within 14 days, and the most common response was a higher vitamin D dose 27.
  • Baseline dialysate calcium and the serum-dialysate gradient did not modify cinacalcet’s effect on cardiovascular events, and dialysate calcium was rarely changed in either arm 28.
  • Etelcalcetide versus cinacalcet (RCT, 683 patients, 26 weeks): decreased blood calcium in 68.9% versus 59.8% (absolute increase 9.1%, NNH 11) 29.

Calcimimetic-induced asymptomatic hypocalcemia is common and usually transient; it is not by itself a reason to move to 3.5 mEq/L. A 3.0 mEq/L bath is a reasonable choice for the calcimimetic-treated patient with a prolonged QTc, symptomatic hypocalcemia, or intradialytic hypotension; that is expert opinion, and no trial tests it. Citrate-acidified dialysate also lowers ionized calcium (section 2) 30.

Selecting within the range

ChooseTypical patientWatch for
2.5 mEq/L (1.25 mmol/L)Calcium-based binder or active vitamin D with high-normal calcium; low PTH or adynamic bone; progressive vascular calcificationHypotension, QTc, post-dialysis perioral tingling or cramps
3.0 mEq/L (1.50 mmol/L)Intradialytic hypotension or cardiomyopathy; long QTc; calcimimetic-related low calcium; low calcium intakeHypercalcemia, PTH over-suppression
3.5 mEq/L (1.75 mmol/L)Not a standing default; short-term only for a specific indication under nephrologist directionCalcium loading and calcification 4,5,6
Below 2.5 mEq/LAvoid outside supervised management of hypercalcemiaArrest, hypotension, heart failure 2,3
Is 1.25 mmol/L “better” than 1.50?

No. KDIGO treats 1.25–1.50 mmol/L as one range because the evidence cannot separate the two 1. Outcome harm signals cluster below 1.25 mmol/L 2,3 and at 1.75 mmol/L 4,5, and one arrhythmia study favors a bath above 1.25 21. Choose within the range by phenotype: hemodynamics, QTc, calcimimetic use, calcium load, and bone turnover.

2. Dialysate bicarbonate, acetate, and citrate

Chemistry and the number on the screen

Bicarbonate dialysate needs a small amount of acid in the acid concentrate, and that acid ends up as acetate (or citrate), which the liver and muscle convert to bicarbonate. The UK guideline recommends the term “dialysate buffer” instead of “dialysate bicarbonate” because manufacturers and machines report different things 7. In the US, two widely used acid concentrates carry 4 and 8 mEq/L of acetate, which adds to the bicarbonate setting 8. In 2012 the FDA classified the manufacturer’s safety notification on these products as a Class 1 recall for risk of alkalosis with acetate-containing acid concentrates 9. The practical lesson: prescribe and audit the total buffer, and know which concentrate the unit uses.

In DOPPS, mean dialysate bicarbonate was 35.5 mEq/L, from 32.2 in Germany to 37.0 in the US, where 45% of patients received 38 mEq/L or more 10.

Outcomes and the alkalosis mechanism

Tentori 2013 (DOPPS, observational): in 17,031 patients from 11 countries, adjusted mortality rose with dialysate bicarbonate, HR 1.08 (1.01–1.15) per 4 mEq/L, and HR 1.07 (0.97–1.19) for 38 or higher versus 33–37. The association held across pre-dialysis bicarbonate levels and in facilities that used a single concentration, and was stronger with longer vintage 10.

Why post-dialysis alkalosis could hurt 31,32,33:

  • Alkalosis increases calcium binding to albumin and lowers ionized calcium, which impairs contractility.
  • A pH above 7.40 increases hemoglobin’s oxygen affinity.
  • Alkalosis shifts potassium into cells. In an 8-patient randomized crossover, serum potassium at 240 minutes was 3.34 mEq/L on a 39 mEq/L bicarbonate bath versus 3.8 on 35 and 4.24 on 27, without a significant difference in total potassium removal 32 (see Dialysate potassium).
  • Post-dialysis bicarbonate rises in proportion to the dialysate concentration and returns to baseline by 44–68 hours, so a high bath does not buy a higher pre-dialysis value 33.

The UK guideline cites a 2011 internal case-control memo from a dialysis provider (941 in-unit cardiac arrests in 2010) in which risk was 4.7 times higher with pre-dialysis bicarbonate above 28 mmol/L and 6.3 times higher if pre-dialysis potassium was also below 4 7; it is a company document, not a peer-reviewed publication. A 2025 systematic review found no randomized trial reporting mortality or hospitalization for dialysate bicarbonate 34.

Pre-dialysis bicarbonate: what to aim for

StudyFinding
Bommer 2004 (DOPPS) 35U-shaped risk: lowest mortality at a midweek pre-dialysis bicarbonate of 20.1–21.0; higher risk above 27 and at 17 or below
Wu 2006 1156,385 patients: unadjusted, mortality rose above 23; after adjusting for malnutrition-inflammation markers, values above 22 carried lower risk. High bicarbonate is a marker of poor protein intake
Yamamoto 2015 3615,132 Japanese patients: pre-dialysis pH of 7.40 or higher associated with mortality (HR 1.36, 1.13–1.65); bicarbonate itself was not
UK Renal Association 2019 7Pre-dialysis bicarbonate 18–26 mmol/L; do not reflexively adjust the dialysate for an abnormal value

Practical approach. Keep the total buffer at or below 37–38 mEq/L for most patients, which with a 4 mEq/L-acetate acid concentrate usually means a bicarbonate setting of 33–35 if the machine display excludes the acetate; confirm the convention for the machines in use 7,8. A high pre-dialysis bicarbonate should prompt a nutrition assessment before a bath change 7,11. Lower the buffer when pairing it with a low-potassium bath or when pre-dialysis potassium is low; the UK guideline identifies higher buffer with low-potassium dialysate as a hazardous pairing 7.

Oral bicarbonate versus bath. For persistent pre-dialysis acidosis despite adequate delivered dialysis, oral sodium bicarbonate spreads alkali across the interdialytic interval instead of concentrating it into a post-dialysis spike. Randomized evidence comparing the strategies on outcomes is very uncertain 34.

Citrate-acidified dialysate

Citrate dialysate replaces acetic acid with citric acid (1.0 mmol/L in the Dutch trials) 30. Citrate chelates calcium and magnesium in the dialyzer, giving a local anticoagulant effect and lowering ionized calcium.

StudyDesignFinding
Kossmann 2009 37142 patients, 6-month switch, before-aftereKt/V 1.51 to 1.57; lower beta-2 microglobulin, BUN, creatinine, phosphate
Schmitz 2016 3892 patients (HD and HDF), randomized crossover, 4 weeks eachLess post-dialysis bicarbonate overcorrection; no difference in severe hypocalcemia or alkalosis; more adverse events (fatigue, muscle spasms, pain) on citrate, 55 vs 41 patients (absolute increase 15.2%, NNH 7 over 4 weeks)
ter Meulen 2019 3918 patients, crossover, 1 week eachCalcification propensity (T50) improved more with citrate at 1.50 mmol/L calcium than with acetate at 1.25 or 1.50
ter Meulen 2021 3013 patientsQTc rose modestly on citrate with 1.50 calcium (427 to 444 ms) and on acetate with 1.25 calcium (431 to 449 ms), not on acetate with 1.50

The Dutch trials were funded by an unrestricted manufacturer grant 30,39, and all endpoints are short-term surrogates.

Citrate dialysate is not citrate anticoagulation

Citrate-acidified dialysate contains about 1 mmol/L of citric acid in place of acetic acid and needs no calcium infusion. Regional citrate anticoagulation, used mainly in CRRT, infuses trisodium citrate before the filter and replaces calcium separately with ionized-calcium monitoring. Descriptions of “citrate dialysate” at 2.5–4.0 mmol/L with post-filter calcium replacement are describing regional anticoagulation.

3. Dialysate magnesium

Ranges and what dialysis does to plasma magnesium

UK units standardized on 0.5 mmol/L (1.0 mEq/L), replacing older 0.25–0.375 and 0.75 mmol/L baths 7; some North American units use 0.375 mmol/L (0.75 mEq/L) 40. Magnesium crosses the membrane easily, and magnesium-free dialysate is poorly tolerated because of cramps 31. In 34 patients dialyzed against 0.5 mmol/L, mean pre-dialysis plasma magnesium was 0.88 mmol/L and fell by 0.10 mmol/L during treatment; plasma magnesium was stable only in patients starting near 0.74 mmol/L, and the authors concluded that current dialysate magnesium may be too low 12.

Observational associations

  • Japanese registry, 142,555 patients: a J-shaped association, with the lowest three sextiles and the highest sextile carrying higher mortality 13.
  • CONTRAST post hoc, 365 European patients: per 0.1 mmol/L higher baseline magnesium, all-cause mortality HR 0.85 (0.77–0.94), cardiovascular mortality 0.73 (0.62–0.85), and sudden death 0.76 (0.62–0.93) 14.
  • MiD loop-recorder study: higher pre-dialysis magnesium was associated with fewer arrhythmias (IRR 0.49 per 1 mg/dL, 0.25–0.94) 21; serum magnesium was not associated with QTc in another cohort 25. Interactions between magnesium and potassium-related risk have been reviewed 41.

Interventional data

StudyDesignInterventionResultEndpoint
Bressendorff 2018 42Double-blind RCT, 57 analyzed, 28 days1.0 to 2.0 mEq/LCalcification propensity (T50) +73 min (30–116); serum magnesium +0.88 mg/dLSurrogate
Del Giorno 2020 43Randomized crossover, 39 patients, 4 weeks0.50 to 0.75 mmol/LPulse-wave velocity −0.91 m/s; systolic BP −12.96 mmHgSurrogate
Jefferies 2020 44Randomized crossover, 20 patients, 2 weeks0.5 vs 1.0 mmol/LNo difference in intradialytic BP fall, cardiac output, or myocardial stunningPhysiologic
Kyriazis 2004 23Crossover, 8 + 14 patients0.25 / 0.5 / 0.75 mmol/L0.75 mmol/L gave the best intradialytic BP stability; 0.25 with calcium 1.25 was a major cause of hypotensionPhysiologic
Schmaderer 2017 45Matched cohort, 25 vs 500.75 vs 0.50 mmol/LAll-cause mortality HR 0.35 (0.13–0.97)Observational, tiny

A 2026 narrative review by the Dial-Mag investigators concluded that higher dialysate or oral magnesium improves vascular surrogates and may lower cardiovascular mortality, but that most trials were small, single-center, short, and surrogate-based 46. Dial-Mag is a pragmatic, registry-based cluster RCT in 137 Canadian centers comparing a center-wide dialysate magnesium of 0.75 mmol/L with 0.5 mmol/L or less, with co-primary outcomes of death or major cardiovascular hospitalization and patient-reported cramps; its trial period ended on 31 March 2026 and results are pending 15. A Dutch feasibility and safety RCT (MAGIC-HD) has a published protocol 47.

Proton pump inhibitors

In 62 veterans dialyzed against 0.75–1.0 mEq/L, PPI users had lower plasma magnesium (1.48 vs 1.65 mEq/L) independent of diet and adequacy 48. In 155 Montreal patients, PPI users averaged 0.93 versus 1.02 mmol/L, and 16% versus 4% were below 0.8 mmol/L 40. With no renal magnesium excretion, the signal is intestinal. Deprescribe the PPI when possible; otherwise check magnesium.

Practical approach

  • Default 1.0 mEq/L (0.5 mmol/L). Avoid lower baths, especially paired with 2.5 mEq/L calcium in hypotension-prone patients 23.
  • Consider 1.5 mEq/L (0.75 mmol/L) case by case while Dial-Mag is pending 15: low pre-dialysis magnesium, an unavoidable PPI, recurrent cramps, peridialytic arrhythmia, or progressive calcification (expert opinion).
  • Watch the other direction: magnesium carbonate binders complicate the choice 31, magnesium-containing laxatives and antacids add load in patients who cannot excrete it, and the highest serum magnesium sextile also carried excess risk in the Japanese registry 13.

4. Dialysate glucose

Why glucose is in the dialysate

The FDA-approved dialysate glucose is 100 mg/dL 31, and UK units have standardized on 5.5 mmol/L 7. Glucose-free dialysate was once common for cost and microbiological reasons, and hypoglycemia followed, particularly in diabetic patients 7. Glucose-free dialysate also removes more potassium, because the absence of insulin-driven intracellular shift leaves more potassium in plasma 31.

Burmeister 2007: 42 patients (21 diabetic) dialyzed on glucose-free and then 90 mg/dL glucose dialysate. Patients with any glucose below 70 mg/dL fell from 10 to 1; none had symptoms; glucose lost to the dialysate fell from 16.7 to 5.2 g/h. That is an RRR of 90%, an ARR of 21.4%, and an NNT of 5 patients per session 16. In a follow-up study, the diabetic patients who became hypoglycemic were those with the lower pre-dialysis glucose (140 vs 278 mg/dL on glucose-free dialysate) 49. A 2026 systematic review and network meta-analysis (39 studies, 2,043 patients) found that low-glucose dialysate reduced the proportion of patients with hypoglycemia compared with glucose-free dialysate (randomized studies OR 0.18, 0.09–0.33, high certainty) and lowered intradialytic hypotension 50.

100 versus 200 mg/dL

In a randomized crossover of 29 patients (14 diabetic), 3 weeks each, 200 mg/dL raised mean intradialytic glucose by 38.8 mg/dL in diabetic and 20.6 mg/dL in non-diabetic patients and raised insulin in non-diabetic patients. Hypoglycemia, potassium, phosphorus, IDWG, and intradialytic events did not differ 17.

Glucose in the dialysate is not a guarantee

In 98 patients with type 2 diabetes on dialysate glucose of 100–150 mg/dL, monitored by continuous glucose monitoring, sensor glucose fell during every treatment, reached a nadir below the dialysate glucose in 50%, and 21% had hemodialysis-related hypoglycemia (below 70 mg/dL during dialysis or between the end of dialysis and the next meal), all asymptomatic 18.

No meaningful osmotic effect

Dialysate glucose of 100 mg/dL contributes about 5.6 mOsm/kg, and 200 mg/dL about 11. Ultrafiltration in hemodialysis is driven by transmembrane pressure, not an osmotic agent; the historical practice of adding glucose for osmotic ultrafiltration ended when pressure-driven ultrafiltration arrived 31. Glucose in hemodialysis dialysate is a hypoglycemia measure, not a volume tool, and KDIGO considers it unlikely to have meaningful blood-pressure effects 26.

Practical approach

  • 100 mg/dL for everyone; 200 mg/dL offers no clear advantage 17.
  • Diabetic patients on insulin or insulin secretagogues: check glucose when pre-dialysis glucose is low, when symptoms occur, and after long sessions; post-session hypoglycemia before the next meal is common and silent 18,49. Medication timing on dialysis days belongs to the prescriber and the diabetes plan.

5. At a glance

ComponentStandard rangeWhen to changeRisks of getting it wrong
Calcium2.5–3.0 mEq/L (1.25–1.50 mmol/L)2.5 for calcium loading or low PTH; 3.0 for IDH, cardiomyopathy, long QTc, calcimimetic hypocalcemiaBelow 2.5: arrest, heart failure, IDH. At 3.5: calcium loading, calcification, mortality signal
Total bufferAt or below 37–38 mEq/LLower with a low-potassium bath, low pre-HD potassium, or high pre-HD bicarbonate; raise cautiously for persistent acidosis after adequacy and nutrition are addressedPost-dialysis alkalosis, potassium shift, low ionized calcium; mortality association with higher bath
Magnesium1.0 mEq/L (0.5 mmol/L)Consider 1.5 mEq/L for low serum magnesium, PPI use, cramps, arrhythmiaToo low: cramps, IDH (especially with low calcium), arrhythmia signal. Too high: hypermagnesemia with magnesium-containing drugs
Glucose100 mg/dL (5.6 mmol/L)Rarely; avoid glucose-freeGlucose-free: silent hypoglycemia, more potassium removal. 200: hyperglycemia and hyperinsulinemia

Evidence gaps

  • Calcium: no trial separates 1.25 from 1.50 mmol/L 1, and no trial has tested a dialysate calcium strategy in calcimimetic-treated patients 28.
  • Buffer: no randomized trial reports mortality or hospitalization 34, and machine and manufacturer terminology makes the observational literature hard to compare 7.
  • Magnesium: all interventional data are surrogate or physiologic 42,43,44,45,46; Dial-Mag has not reported 15.
  • Glucose: the optimal concentration for insulin-treated patients under continuous glucose monitoring, and management of post-session hypoglycemia, are undefined 18.

At the chair

For dialysis nurses and technicians

Read calcium on the acid concentrate label with its unit; 2.5 mEq/L and 1.25 mmol/L are the same bath. Know whether the machine’s bicarbonate number includes the acetate from the acid concentrate, because the patient receives both. A calcium bath below 2.5 mEq/L or at 3.5 mEq/L is not a routine prescription. Diabetic patients on insulin can become hypoglycemic during or after treatment without symptoms.

Nursing card N2: Dialysate prescription check — do this, call when, don’t, and why

The physician’s written order and the unit protocol always govern.

Also in this module

References

References are carried from a reference-checked evidence review (September 2026) and renumbered for this page. Each was checked against its PubMed record, full text, or the issuing agency’s document.

  1. Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work Group. KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl. 2017;7(1):1-59. PMID: 30675420
  2. Pun PH, Horton JR, Middleton JP. Dialysate calcium concentration and the risk of sudden cardiac arrest in hemodialysis patients. Clin J Am Soc Nephrol. 2013;8(5):797-803. PMID: 23371957
  3. Brunelli SM, Sibbel S, Do TP, Cooper K, Bradbury BD. Facility dialysate calcium practices and clinical outcomes among patients receiving hemodialysis: a retrospective observational study. Am J Kidney Dis. 2015;66(4):655-665. PMID: 26015274
  4. Kim HW, Kim SH, Kim YO, et al. Impact of dialysate calcium concentration on clinical outcomes in incident hemodialysis patients. Medicine (Baltimore). 2015;94(40):e1694. PMID: 26448019
  5. Ok E, Asci G, Bayraktaroglu S, et al. Reduction of dialysate calcium level reduces progression of coronary artery calcification and improves low bone turnover in patients on hemodialysis. J Am Soc Nephrol. 2016;27(8):2475-2486. PMID: 26701977
  6. Gotch FA, Kotanko P, Thijssen S, Levin NW. The KDIGO guideline for dialysate calcium will result in an increased incidence of calcium accumulation in hemodialysis patients. Kidney Int. 2010;78(4):343-350. PMID: 20520595
  7. Ashby D, Borman N, Burton J, et al. Renal Association Clinical Practice Guideline on Haemodialysis. BMC Nephrol. 2019;20(1):379. PMID: 31623578
  8. Smith WB, Gibson S, Newman GE, et al. The dynamics of the metabolism of acetate and bicarbonate associated with use of hemodialysates in the ABChD trial: a phase IV, prospective, single center, single blind, randomized, cross-over, two week investigation. BMC Nephrol. 2017;18(1):273. PMID: 28851317
  9. US Food and Drug Administration. Class 1 Device Recalls: Fresenius GranuFlo (powder) Acid Concentrate and Fresenius NaturaLyte Liquid Acid Concentrate. Initiated 2012-03-29; manufacturer-stated reason "Risk of Alkalosis with acetate containing dialysis acid concentrates"; terminated 2017-07-20.
  10. Tentori F, Karaboyas A, Robinson BM, et al. Association of dialysate bicarbonate concentration with mortality in the Dialysis Outcomes and Practice Patterns Study (DOPPS). Am J Kidney Dis. 2013;62(4):738-746. PMID: 23707043
  11. Wu DY, Shinaberger CS, Regidor DL, McAllister CJ, Kopple JD, Kalantar-Zadeh K. Association between serum bicarbonate and death in hemodialysis patients: is it better to be acidotic or alkalotic? Clin J Am Soc Nephrol. 2006;1(1):70-78. PMID: 17699193
  12. Leenders NHJ, van Ittersum FJ, Hoekstra T, Hoenderop JGJ, Vervloet MG. Routine hemodialysis induces a decline in plasma magnesium concentration in most patients: a prospective observational cohort study. Sci Rep. 2018;8(1):10256. PMID: 29980722
  13. Sakaguchi Y, Fujii N, Shoji T, Hayashi T, Rakugi H, Isaka Y. Hypomagnesemia is a significant predictor of cardiovascular and non-cardiovascular mortality in patients undergoing hemodialysis. Kidney Int. 2014;85(1):174-181. PMID: 23986148
  14. de Roij van Zuijdewijn CL, Grooteman MP, Bots ML, et al. Serum magnesium and sudden death in European hemodialysis patients. PLoS One. 2015;10(11):e0143104. PMID: 26600017
  15. Dial-Mag Investigator Writing Committee; Killin L, Bohm C, et al. Outcomes of adopting a higher versus lower concentration of hemodialysate magnesium as a center-wide policy (Dial-Mag): a clinical research protocol of a pragmatic, registry-based, cluster randomized trial. Can J Kidney Health Dis. 2025;12:20543581251385011. PMID: 41393273
  16. Burmeister JE, Scapini A, da Rosa Miltersteiner D, da Costa MG, Campos BM. Glucose-added dialysis fluid prevents asymptomatic hypoglycaemia in regular haemodialysis. Nephrol Dial Transplant. 2007;22(4):1184-1189. PMID: 17272314
  17. Raimann JG, Kruse A, Thijssen S, et al. Metabolic effects of dialyzate glucose in chronic hemodialysis: results from a prospective, randomized crossover trial. Nephrol Dial Transplant. 2012;27(4):1559-1568. PMID: 21940484
  18. Hayashi A, Shimizu N, Suzuki A, et al. Hemodialysis-related glycemic disarray proven by continuous glucose monitoring; glycemic markers and hypoglycemia. Diabetes Care. 2021;44(7):1647-1656. PMID: 34045240
  19. Ketteler M, Evenepoel P, Holden RM, et al. Chronic kidney disease-mineral and bone disorder: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2025;107(3):405-423. PMID: 39864017
  20. Pun PH, Lehrich RW, Honeycutt EF, Herzog CA, Middleton JP. Modifiable risk factors associated with sudden cardiac arrest within hemodialysis clinics. Kidney Int. 2011;79(2):218-227. PMID: 20811332
  21. Tumlin JA, Roy-Chaudhury P, Koplan BA, et al. Relationship between dialytic parameters and reviewer confirmed arrhythmias in hemodialysis patients in the Monitoring in Dialysis study. BMC Nephrol. 2019;20(1):80. PMID: 30836948
  22. van der Sande FM, Cheriex EC, van Kuijk WH, Leunissen KM. Effect of dialysate calcium concentrations on intradialytic blood pressure course in cardiac-compromised patients. Am J Kidney Dis. 1998;32(1):125-131. PMID: 9669433
  23. Kyriazis J, Kalogeropoulou K, Bilirakis L, et al. Dialysate magnesium level and blood pressure. Kidney Int. 2004;66(3):1221-1231. PMID: 15327421
  24. Näppi SE, Virtanen VK, Saha HH, Mustonen JT, Pasternack AI. QTc dispersion increases during hemodialysis with low-calcium dialysate. Kidney Int. 2000;57(5):2117-2122. PMID: 10792632
  25. Kim ED, Watt J, Tereshchenko LG, et al. Associations of serum and dialysate electrolytes with QT interval and prolongation in incident hemodialysis: the Predictors of Arrhythmic and Cardiovascular Risk in End-Stage Renal Disease (PACE) study. BMC Nephrol. 2019;20(1):133. PMID: 30999887
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