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Does hemodialysis dialysate potassium composition matter?

Potassium is an essential electrolyte, and dyskalemia can cause life-threatening arrhythmias and even death, particularly among persons with compromised renal function and those undergoing hemodialysis. In a study of emergency medical hospital admissions, Conway, Creagh, Byrne, O'Riordan, and Silke (2015) found that patients with hyperkalemia on admission had greater than five times the risk for in-hospital mortality, were sicker, and were older than normokalemic patients.

Potassium is critical to cardiac function. It is primarily found within cells. The extracellular concentration is 3.5 to 5.0 mEq/L, while the intracellular concentration is 150 to 160 mEq/L (Huether, 2012). The extracellular levels of potassium are measured in serum blood tests and are the levels evaluated for normalcy. The distribution of potassium between the intra- and extra-cellular spaces is affected by insulin, beta-2 adrenergic receptors in the sympathetic nervous system, and acid-base status (Clarkson & Brenner, 2005). The kidney is the most sophisticated regulator of potassium in the body, with 90% of reabsorption occurring in the proximal tubule and loop of Henle (Huether, 2012). Renal excretion of potassium occurs in the distal nephron and is affected by the reninangiotensin-aldosterone system, vasopressin, and dietary potassium intake (Clarkson & Brenner, 2005). Medications can affect the potassium level. Medications, such as insulin and glucose, sodium polystyrene sulfonate, sodium bicarbonate, fludrocortisone, thiazide and loop diuretics, and the beta 2 agonist albuterol, are known to lower potassium levels, while angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone agonists, and beta-2 antagonists raise potassium levels (Kjeldsen, 2010; Sanghavi, Whiting, & Uribarri, 2013).

Clinical Question

Is there an impact on sudden cardiac death in patients on hemodialysis as a result of varying dialysate potassium composition? To answer this question, a literature review using Academic Search Complete with the search terms dialysate and potassium was conducted. Only peer-reviewed articles were considered for this review. Eighty-eight articles published between 2001 and 2015 were found, and after a title review, 15 were considered for further review. Of these, five were review articles, three were case-control/cohort studies, one was a pilot study, one was a randomized multicenter prospective study, three were crossover design, and two were editorials.

The Early Years of Dialysate Exploration

Early exploration into the phenomenon of sudden cardiac arrest in patients undergoing hemodialysis revealed a rate of 7 per 100,000 hemodialysis sessions (Kamik et al, 2001). In this case-cohort study by Karnik and colleagues (2001), patients who experienced cardiac arrest were twice as likely to be dialyzed with a 0 or 1.0 mEq/L potassium dialysate than those in the cohort. Karnik et al. (2001) did not find a correlation between the dialysate prescription and the pre-dialysis serum potassium or timing of the cardiac arrest, but did note that only 17.8% of patients prescribed the low dialysate potassium had a pre-hemodialysis serum potassium of 5.0 mEq/L or higher, and only 4% were above 6.0 mEq/L. They postulated that the combination of a low dialysate concentration and low pre-dialysis serum potassium contributed to the incidence of sudden cardiac arrest in the dialysis unit.

In a crossover design study by Sangthawan, Atkins, and Kerr (2001) to determine adequacy of dialysis at two potassium concentrations, no significant difference in ultrafiltration volume was found between dialyzing with a 1 mmol/L potassium dialysate or a 2 mmol/L potassium dialysate. Only dialysate concentration of 3 mmol/L was found to significantly impact ultrafiltration. Sangthawan et al. (2001) concluded that the length of the dialysis session was more important than the dialysate composition in determining effectiveness of urea reduction and rebound.

The Mid Years of Dialysate Exploration

By the late 2000s, two additional studies were conducted that examined the impact of constant dialysate potassium concentration versus potassium profiling and cardiac arrhythmias. Munoz et al. (2008) in a pilot study and Santoro et al. (2008) in a crossover single blind design study found no statistical difference in post-procedure potassium levels. Both methods were safe and well tolerated by patients, and there was a reduction of arrhythmias in patients who were in the potassium profiling group. Both studies suggest that potassium profiling may be the safer option for those prone to arrhythmias in an effort to reduce the early drop in potassium levels.

In an attempt to better understand potassium removal during hemodialysis, Ciandrini and colleagues (2009) also dialyzed 34 patients first for two weeks with constant dialysate potassium, then for two weeks with potassium profiling. Electrolytes were measured at various times throughout the hemodialysis session and at the end of the session. A mathematical model of potassium removal was created, and the results of the study indicated no significant difference in the timing of removal of potassium during the two methods. They did find, however, that when potassium levels are between 4 and 5 mmol/L, the sodium-potassium pump, which moves potassium from the extracellular to the intracellular space, is most active during the first 60 minutes of hemodialysis. When the potassium level drops below 4 mmol/L, usually after approximately 90 minutes, plasma concentration of potassium remains virtually constant, with the majority of potassium removal coming from the intracellular spaces. After dialysis, the potassium rebounds in the extracellular space, returning the concentration to the pre-dialysis level.

The Late Years of Dialysate Exploration

From 2010 through 2015, five reviews and six research studies were published that continued to look at modifiable risk factors for cardiac arrhythmias and sudden cardiac arrest in patients undergoing hemodialysis. In 2010, Kjeldsen published a review of the causes of hypokalemia and sudden cardiac death. He reported the incidence of hypokalemia in hospitalized patients approaches 20% and may be as high as 40% in those on diuretics. Kjeldsen (2010) also reported that hypokalemia is associated with an increase in cardiac arrhythmias, and that the lower the serum potassium level, the higher the risk of arrhythmias.

In 2010, Phipps and Harris published a review summarizing current evidence for dialysate modelling that supported potassium modelling or a higher potassium dialysate concentration in patients susceptible to arrhythmias and post-dialysis rebound hypertension. In 2011, Pun, Lehrich, Honeycutt, Herzog, and Middleton published the results of their case-control study that focused on modifiable elements in the hemodialysis prescription. In a multivariable logistic regression model, they found that a potassium dialysate composition less than 2 mEq/L resulted in a more than double increase in the risk of sudden cardiac arrest, and they did not find any benefit to using a low potassium dialysate for any predialysis serum potassium level.

In a retrospective study conducted by Hwang, Wang, Chan, and Chen (2011), patients on hemodialysis with hypokalemia had a higher mortality rate than those experiencing hyperkalemia. Additionally, they found that those with hypokalemia were more malnourished with a lower serum albumin, BUN, and phosphorus concentration, and had a higher inflammatory state, contributing to their higher mortality rates. Recognizing that there are other correlates to cardiac arrest besides dialysate potassium composition, Flythe and colleagues (2014) confirmed that lower albumin, body mass index (BMI), and dialysate potassium were associated with greater incidence of cardiac arrest, and suggested that use of low potassium dialysate be limited.

Agar, Culleton, Fluck, and Leypoldt (2015) confirmed the rapid decrease in potassium during the early phase of hemodialysis, and the subsequent rebound following dialysis. They found large variability between patients in terms of potassium clearance, thus complicating the decision about the type of dialysate to use. Clearly, low dialysate potassium has been presented as a significant risk factor for sudden cardiac arrest and cardiac arrhythmias. In two separate reviews, Moledina and Geller (2014) and Abuelo (2015) summarized the incidence of hypo- and hyperkalemia in patients on hemodialysis, and the rates for sudden cardiac death and arrhythmias. Both sets of authors raise the important consideration of specific patient factors, such as other co-morbidities, serum albumin, pre-dialysis potassium level, nutritional status, and other factors affecting serum potassium, such as medications and dietary intake.


Optimizing potassium removal during hemodialysis while reducing patients' risk for cardiac arrhythmias and sudden cardiac arrest has been an area of investigation for the past 15+ years. Researchers have identified the complexity of potassium removal during hemodialysis because of the movement of potassium into and out of cells. Studies have shown that the greatest decrease in serum potassium levels occurs during the first two to three hours of dialysis, and then rebounds post-hemodialysis, regardless of the potassium dialysate concentration, although the lower the dialysate potassium concentration, the greater the removal of potassium during the hemodialysis treatment (Agar et al., 2015).

As more was known about potassium kinetics and dialysate potassium, researchers began to explore whether there were other predictors of cardiac events, such as coronary artery disease, medications, dietary potassium intake, and overall health status of the individual. Jain and colleagues (2012) identified that the stage of chronic kidney disease, the presence of diabetes mellitus, coronary artery disease, or peripheral vascular disease increased the odds of hyperkalemia and mortality, with stage of chronic kidney disease being the most significant factor. Persons undergoing hemodialysis who missed or shortened their dialysis treatments also had a higher incidence of cardiac arrest and were generally older and sicker than their counterparts who did not have cardiac events (Flythe et al., 2014).

Dialysate potassium modeling has been suggested as a means to maximize potassium removal during hemodialysis while at the same time minimizing cardiac complications. Ciandrini and colleagues (2009) reported that the potassium dialysate concentration influences the action of the sodium-potassium pump, which plays an important role in potassium kinetics. Recognizing the variability in timing of assessing pre-hemodialyis serum potassium levels, researchers are unable to definitively recommend one potassium dialysate concentration over another. Researchers suggest that those at greater risk for cardiac arrhythmia or arrest be carefully monitored with thoughtful consideration of the most appropriate potassium dialysate concentration (Ciandrini et al., 2009; Munoz et al., 2008; Phipps & Harris, 2010; Pun et al., 2011; Sangthawan et al., 2001; Santoro et al., 2008).

Implications for Nursing Practice

Maintaining stable potassium is critical to reduce the incidence of dyskalemia in patients undergoing hemodialysis. Nurses and advance practice nurses are an integral part of the team to accurately monitor pre-dialysis serum potassium levels, nutritional status, co-morbidities, medications, and dietary potassium intake. Modelina and Geller (2014) suggest that an optimal pre-dialysis potassium is approximately 5 mEq/L, and patients with the lowest mortality had a potassium level between 4.6 and 5.3 mEq/L. Sanghavi and colleagues (2013) believe that every patient on hemodialysis should have access to a renal nutritionist/dietitian. Furthermore, nephrology nurses should conduct a medication review to assess whether the patient is on medications that may contribute to hyperkalemia, such as ACE Inhibitors, angiotensin II receptor blockers, potassium-sparing diuretics, or medications that may contribute to hypokalemia, such as fludrocortisone, furosemide, or sodium polystyrene sulfonate. Keen attention should also be given to assessing the patient's bowel function because constipation can contribute to hyperkalemia. Patient education about ways to reduce dietary potassium should also be provided at every opportunity. Encouraging patients to not miss hemodialysis treatments or reduce the time on treatment should also be emphasized for optimum potassium removal. No specific recommendations can be made regarding the dialysate potassium concentration due to the complexity of factors affecting potassium balance and potassium removal.


The purpose of this article is to review the literature related to hemodialysis dialysate potassium concentration on sudden cardiac death.


1. Identify the role and importance of potassium in cardiac function.

2. Discuss the evolution of knowledge related to varying potassium dialysate concentrations on reducing the risk of sudden cardiac death in persons on hemodialysis.

3. Relate dietary and pharmacologic factors affecting serum potassium levels to the complexity of determining the appropriate potassium dialysate concentration.

Exploring the Evidence is a department in the Nephrology Nursing Journal designed to provide a summary of evidence-based research reports related to contemporary nephrology nursing practice issues. Content for this department is provided by members of the ANNA Research Committee. Committee members review the current literature related to a clinical practice topic and provide a summary of the evidence and implications for best practice. Readers are invited to submit questions or topic areas that pertain to evidence-based nephrology practice issues. Address correspondence to: Tamara Rear, Exploring the Evidence Department Editor, ANNA National Office, East Holly Avenue/Box 56, Pitman, NJ 08071-0056; (856) 256-2320; or via e-mail at The opinions and assertions contained herein are the private views of the contributors and do not necessarily reflect the views of the American Nephrology Nurses' Association.


Abuelo, J.G. (2015). Low dialysate potassium concentration: An overrated risk factor for cardiac arrhythmia? Seminars in Dialysis, 28(3), 266-275. doi: 10.111 l/sdi.12337

Agar, B., Culleton, B., Fluck, R., & Leypoldt, J. (2015). Potassium kinetics during hemodialysis. Hemodialysis International, 19(1), 23-32. doi: 10.1111/hdi.12195

Ciandrini, A., Seven, S., Cavalcanti, S., Fontanazzi, F., Grandi, F, Buemi, M., ... Santoro, A. (2009). Model-based analysis of potassium removal during hemodialysis. Artificial Organs, 33(10), 835-843. doi:lO.1111/j.1525-1594.2009.00806.x

Clarkson, M.R., & Brenner, B.M. (2005). Disorders of potassium balance. In M. Clarkson & B. Brenner (Eds). Pocket companion to Brenner & Rector's the kidney (7th ed., pp. 93-110). Philadelphia, PA: Elsevier.

Conway, R., Creagh, D., Byrne, D., O'Riordan, D., & Silke, B. (2015). Serum potassium levels as an outcome determinate in acute medical admissions. Clinical Medicine, 75(3), 239-243.

Flythe, J., Li, N., Lin, S., Brunelli, S., Hymes, J., & Lacson, E. (2014). Associates of cardiopulmonary arrest in the perihemodialytic period. International Journal of Nephrology, 2014, 1-12. doi: 10.1155/2014/961978

Huether, S. (2012). Fluids and electrolytes, acids and bases. In S. Huether, & K. McCance (Eds.), Understanding pathophysiology (5th ed., pp. 98-117). St. Louis, MO: Elsevier.

Hwang, J., Wang, C., Chen, C., & Chen, H. (2011). Hypokalemia is associated with increased mortality rate in chronic hemodialysis patients. Blood Purification, 32(4), 254-261. doi: 10.1159/000325226

Jain, N., Kotla, S., Little, B., Weideman, R., Brilakis, E., Reilly, R., & Baheijee, S. (2012). Predictors of hyperkalemia and death in patients with cardiac and renal disease. American Journal of Cardiology, 705(10), 1510-1513. doi:10.1016/j.amjcard.2012.01.367

Kamik, J.A., Young, B.S., Lew, N.L., Herget, M., Dubinsky, C. Laarus, J.M., & Chertow, G.M. (2001). Cardiac arrest and sudden death in dialysis units. Kidney International, 50(1), 350-357.

Kjeldsen, K. (2010). Hypokalemia and sudden cardiac death. Experimental and Clinical Cardiology, 75(4), e96-e99.

Moledina, D., & Geller, D. (2014). Is low dialysate potassium ever indicated in outpatient hemodialysis? Seminars in Dialysis, 27(3), 263-265. doi: 10.1111/sdi.12212

Munoz, R., Montenegro, J., Salcedo, A., Gallardo, I., Martinez, L, Quintanilla, N., ... Lekuona, I. (2008). Effect of acetate-free biofiltration with a potassium-profiled dialysate on the control of cardiac arrhythmias in patients at risk: A pilot study. Hemodialysis International, 72(1), 108-113. doi: 10.1111/j.15424758.2008.00250.x

Phipps, L., & Harris, D. (2010). Review: Modelling the dialysate. Nephrology, 75(4), 393-398. doi: 10.1111/j.1440-1797.2010.01299.x

Pun, R, Lehrich, R., Honeycutt, E., Herzog, C., & Middleton, J. (2011). Modifiable risk factors associated with sudden cardiac arrest within hemodialysis clinics. Kidney International, 79(2), 218-227. doi: 10.1038/ki.2010.315

Sanghavi, S., Whiting, S., & Uribarri, J. (2013). Potassium balance in dialysis patients. Seminars in Dialysis, 26(5), 597-603. doi: 10.1111/sdi.12123

Sangthawan, R, Atkins, R., & Kerr, P. (2001). Comparison of dialysis adequacy at two dialysate potassium concentrations. Nephrology, 6(2), 89-91.

Santoro, A., Mancini, E., London, G., Mercadal, L., Fessy, H., Perrone, B, ... Cavalcanti, S. (2008). Patients with complex arrhythmias during and after haemodialysis suffer from different regimens of potassium removal. Nephrology Dialysis Transplantation, 23(4), 1415-1421. doi:10.1093/ndt/gfm730

This offering for 1.3 contact hours is provided by the American Nephrology Nurses' Association (ANNA).

American Nephrology Nurses' Association is accredited as a provider of continuing nursing education by the American Nurses Credentiaiing Center Commission on Accreditation.

ANNA is a provider approved by the California Board of Registered Nursing, provider number CEP 00910.

This CNE article meets the Nephrology Nursing Certification Commission's (NNCC's) continuing nursing education requirements for certification and recertification.

Mary S. Haras, PhD, MBA, APN, NP-C, CNN, is an Associate Professor and Associate Dean for Graduate Nursing Programs, Saint Xavier University School of Nursing, Chicago, IL; Chair, ANNA's Research Committee; and a member of ANNA's Windy City Chapter. She can contacted directly via email at

Statement of Disclosure: The authors reported no actual or potential conflict of interest in relation to this continuing nursing education activity.

Note: Additional statements of disclosure and instructions for CNE evaluation can be found on page 581.
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Title Annotation:Exploring the Evidence
Author:Haras, Mary S.
Publication:Nephrology Nursing Journal
Article Type:Report
Geographic Code:1USA
Date:Nov 1, 2015
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