Sections

Treatment

Approach Considerations

The aggressiveness of therapy for hyperkalemia is directly related to the rapidity with which the condition has developed, the absolute level of serum potassium, and the evidence of toxicity. The faster the rise in the potassium level, the higher it has reached, and the greater the evidence of cardiotoxicity, the more aggressive therapy should be.

If the patient has only a moderate elevation in potassium level and no electrocardiographic (ECG) abnormalities, excretion can be increased by using a cation exchange resin or diuretics, and the source of excess potassium (eg, increased intake or inhibited excretion) can be corrected.^[65]

In patients with severe hyperkalemia, treatment focuses on immediate stabilization of the myocardial cell membrane, rapid shifting of potassium to the intracellular space, and total body potassium elimination. In addition, all sources of exogenous potassium should be immediately discontinued; including intravenous (IV) and oral potassium supplementation, total parenteral nutrition, and any blood product transfusion. Drugs associated with hyperkalemia should also be discontinued (see Etiology).^[66]

Definitive therapy is hemodialysis in patients with kidney failure or when pharmacologic therapy is not sufficient. Any patient with significantly elevated potassium levels should undergo dialysis; pharmacologic therapy alone is not likely to bring about adequate reduction of potassium levels in a timely fashion.

After emergency management and stabilization of hyperkalemia, the patient should be hospitalized. Once the potassium level is restored to normal, the potassium-lowering therapies can be discontinued, and the serum potassium level can be monitored. Continuous cardiac monitoring should be maintained.

Further workup should be initiated to determine the inciting cause and to prevent future episodes. Such a workup should include evaluation of sources of potassium intake, causes for decreased renal excretion, and causes for decreased cell uptake of potassium. In most cases, all 3 of those etiologic factors contribute to hyperkalemia. It is particularly important to reevaluate the use of potassium supplements (including salt substitutes) in patients with kidney insufficiency or in patients taking medications that impair renal excretion of potassium.

Initial Emergency Management

In the prehospital setting, a patient with known hyperkalemia or a patient with kidney failure with suspected hyperkalemia should have IV access established and should be placed on a cardiac monitor.^[22]In patients with hypotension or marked QRS widening, IV bicarbonate, calcium, and insulin given together with 50% dextrose may be appropriate (see Medication). If digoxin toxicity is suspected, avoid calcium; instead, give magnesium sulfate (2 g over 5 minutes) for patients with cardiac arrhythmias from digitalis toxicity.

In the emergency department (ED), perform continuous ECG monitoring with frequent vital sign checks when hyperkalemia is suspected or when laboratory values indicative of hyperkalemia are received. Measurement of potassium levels at least 1, 2, 4, 6, and 24 hours after identification and treatment of hyperkalemia is recommended.^[66]

Discontinue any potassium-sparing drugs or dietary potassium. If the patient is taking digoxin, look for evidence of digitalis toxicity.

If the hyperkalemia is severe (potassium >7.0 mEq/L) or if the patient is symptomatic, begin treatment before diagnostic investigation of the underlying cause. Individualize treatment in accordance with the patient’s presentation, potassium level, and electrocardiographic findings. For example, patients with mild hyperkalemia may not need anything more than enhancement of potassium excretion.

Medications such as calcium, insulin, glucose, and sodium bicarbonate are temporizing measures. Definitive loss of excess potassium can be achieved only with cation exchange resins, dialysis, or increased renal excretion. Begin administration of a cation exchange resin soon after the other drugs have been administered.

Watch for overcorrection of the potassium level. For example, in diabetic ketoacidosis (DKA) and many other types of metabolic acidosis, the extracellular potassium level is elevated, yet the patient may have a total body deficit of potassium. Once the clinician initiates therapy for DKA, the extracellular potassium level decreases spontaneously.

Pharmacologic Therapy and Dialysis

Medical treatment of hyperkalemia may be conveniently divided into discrete components. Although these different aspects of hyperkalemia treatment are listed sequentially below, in a step-by-step format, they generally are addressed simultaneously.

Step 1

Administer intravenous (IV) calcium to ameliorate cardiac toxicity, if present. Infuse calcium chloride or calcium gluconate (10 mL of a 10% solution over 2-3 minutes). Onset of action occurs within minutes; duration of action is 30 minutes to an hour.^[67]

Step 2

Identify and remove sources of potassium intake. Discontinue oral and parenteral potassium supplements. Remove potassium-containing salt substitutes. Examine the patient’s diet. Change the diet to a low-potassium tube feed or a 2-g potassium ad-lib diet.

Step 3

Enhance potassium uptake by cells to decrease the serum concentration. IV glucose and insulin infusions are very effective in enhancing potassium uptake. A typical regimen is 10 U of regular insulin and 50 mL of dextrose 50% in water (D50W).The onset of action is within 20-30 minutes, and the duration is variable, ranging from 2 to 6 hours. Continuous infusions of insulin and glucose-containing IV fluids can be used for prolonged effect.

IV insulin (even when administered with dextrose) can cause hypoglycemia. Patients with acute kidney injury and chronic kidney disease are especially susceptible, particularly those with lower body weight and creatinine clearance.^[68]Sufficient dextrose in the treatment regimen can minimize the risk. Measure glucose and potassium levels every 2 hours. Continue monitoring glucose levels for at least 6 hours after administering insulin-glucose.^[69]In patients with salt-wasting congenital adrenal hyperplasia, who are at increased risk of hypoglycemia during acute illness, corticosteroid and mineralocorticoid supplementation is necessary.

A retrospective study by Pierce et al of 149 patients with low estimated glomerular filtration rate (eGFR) who received IV insulin for hyperkalemia found no significant difference in the rate of hypoglycemia (blood glucose ≤70 mg/dL) or severe hypoglycemia (< 50 mg/dL) with 10 U versus 5 U of insulin. Rates of hypoglycemia in the 10-U and 5-U groups were 16.7% and 19.7%, respectively (P = 0.79). Rates of severe hypoglycemia were 8.9% and 7.0%, respectively (P = 0.90). ^[70]

Correct metabolic acidosis with sodium bicarbonate. Because of the variable effect of different forms of metabolic acidosis on the serum potassium level, this therapeutic modality is less effective and less predictable in producing a hypokalemic response, especially in patients with chronic renal failure. Nonetheless, if the acidosis is severe, then a trial of parenteral sodium bicarbonate therapy is warranted.

Beta-adrenergic agonists also are quite effective but are perhaps somewhat more controversial and more likely to produce side effects. In the United States, the most commonly used preparation is nebulized albuterol. The dose for treating hyperkalemia, 10 mg, is substantially higher than the usual dose for the treatment of bronchospasm and requires the assistance of a respiratory therapist. The peak hypokalemic effect occurs at 90 minutes. This therapy is highly effective and is preferred to alkali therapy in patients with renal failure.

Parenteral isoproterenol and albuterol also decrease potassium. However, isoproterenol is not commonly used, and parenteral albuterol is not available in the United States. Some investigators have reported tachycardia and chest discomfort with the use of beta-agonist therapy for hyperkalemia. Discontinue beta-adrenergic antagonists.

Step 4

Increase potassium excretion from the body. Renal excretion is enhanced easily in patients with normal kidney function by administering IV saline accompanied by a loop diuretic (eg, furosemide). Discontinue potassium-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBs), and other drugs that inhibit renal potassium excretion. Monitor volume status and aim to maintain euvolemia.

Renal excretion can be enhanced by administration of an aldosterone analogue, such as 9-alpha fluorohydrocortisone acetate. Fluorohydrocortisone is especially helpful in patients with hyporeninemia or hypoaldosteronism. It has been increasingly used in solid-organ transplant recipients who have chronic hyperkalemia from calcineurin inhibitor use. Usually, serum potassium returns to normal after about 48 hours.^[71]

Sodium polystyrene sulfonate

Gastrointestinal (GI) excretion can be increased through the use of cation exchange resins such as sodium polystyrene sulfonate (SPS). SPS can be administered orally or rectally (as a retention enema). Because the major site of action for this drug is the colon, rectal administration is preferred for hyperkalemic emergencies. The effectiveness of SPS is enhanced if the enema can be retained for 1 hour.

SPS is not useful for acute control of hyperkalemia, because its effect on potassium is delayed for at least 2 hours, peaking at 4-6 hours. SPS can decrease serum potassium by 2 mEq/L.

Oral SPS is useful in patients with advanced renal failure who are not yet on dialysis or transplant candidates. One or more daily doses of 15 g can control mild to moderate hyperkalemia effectively, with little inconvenience to patients.

Although SPS has a long history of use for hyperkalemia, its safety and efficacy have been questioned.^{[69, 72, 73, 65]}The US Food and Drug Administration (FDA) advises against its use in patients who do not have normal bowel function (eg, postoperative patients who have not had a bowel movement since their procedure) or those who are at risk for constipation or impaction.^[74]SPS should be discontinued in patients who become constipated, and repeat doses should not be given to patients who have not passed a bowel movement.

In addition, the FDA cautions that giving SPS with sorbitol, an osmotic cathartic used to prevent fecal impaction from SPS and to speed delivery of resin to the colon, has been associated with cases of intestinal necrosis, some of them fatal.^[74]Current evidence indicates that this serious side effect can occur with SPS even when preparation does not contain any sorbitol.^[75]

Patiromer

Patiromer sorbitex calcium (Veltassa) is a nonabsorbed, cation exchange polymer that contains a calcium-sorbitol counterion. It increases fecal potassium excretion by binding potassium in the lumen of the GI tract. It is indicated for hyperkalemia in patients aged 12 years and older. It should not be used as an emergency treatment for life-threatening hyperkalemia because of its delayed onset of action.

FDA approval of patiromer was based on the AMETHYST-DN trial. Results showed that in patients with hyperkalemia and diabetic kidney disease taking renin-angiotensin-aldosterone system inhibitors (RAASi), which are known to cause elevated serum potassium levels, patiromer resulted in statistically significant decreases in serum potassium level after 4 weeks of treatment, lasting through 52 week.^[76]

The OPAL-HK trial showed that patiromer was well tolerated, decreased serum K(+) , and, compared with placebo, reduced recurrent hyperkalemia in patients with chronic kidney disease (CKD) and heart failure who were hyperkalemic while taking RAASi. In the study, patiromer was given to patients with CKD who were taking RAASi and had serum K(+) levels >5.1 mEq/L to < 6.5 mEq/L (n=243) for 4 weeks. Patients whose K(+) levels were ≥3.8 mEq/L to < 5.1 mEq/L at the end of week 4 entered an 8-week randomized withdrawal phase and were randomly assigned to continue patiromer or switch to placebo.^[77]

The primary efficacy endpoint was the between-group difference in median change in the serum K(+) over the first 4 weeks of the withdrawal phase. The median increase in serum K(+) from baseline of the withdrawal phase was greater with placebo (n = 22) than patiromer (n = 27) (P < 0.001). Recurrent hyperkalemia (serum K(+) ≥5.5 mEq/L) occurred in 52% of patients on placebo and 8% of those on patiromer (P < 0.001).^[77]

Patiromer has been proposed for use in the management of acute hyperkalemia in the ED. In an open-label pilot study, 30 patients with severe acute hyperkalemia were randomized to receive standard of care (SOC) or a single dose of 25.2 g oral patiromer in addition to SOC. At 2 hours post-treatment, the serum potassium was lower in the patients in the patiromer arm than in the SOC-only arm. However, no differences were seen between the groups at 6 hours post-treatment.^[78]

In the DIAMOND trial, patiromer helped prevent hyperkalemia in patients with heart failure and reduced ejection fraction who were taking an RAASi and a mineralocorticoid receptor antagonist (spironolactone or eplerenone). On median follow-up of 27 weeks, the adjusted mean increase in serum potassium was 0.03 mmol/L in patients using patiromer (n=439), compared with 0.13 mmol/L in the patients randomized to placebo (n=439). Patients using patiromer were also more likely to be able to reduce their mineralocorticoid receptor antagonist dose.^[79]

Sodium zirconium cyclosilicate

Sodium zirconium cyclosilicate (Lokelma) is approved by the FDA for treatment of hyperkalemia in adults. It preferentially captures potassium in exchange for hydrogen and sodium, which reduces the free potassium concentration in the lumen of the GI tract and thereby lowers the serum potassium level. Like patiromer, sodium zirconium cyclosilicate should not be used as an emergency treatment for life-threatening hyperkalemia because of its delayed onset of action.

Approval was based on the HARMONIZE clinical trial in patients with serum potassium levels of 5.1 mEq/L or higher. In the open-label phase, serum potassium levels declined from 5.6 mEq/L at baseline to 4.5 mEq/L at 48 hours. Median time to normalization was 2.2 hours, with 84% of patients achieving normokalemia by 24 hours and 98% by 48 hours. In the randomized phase, serum potassium was significantly lower during days 8-29 with all 3 zirconium cyclosilicate doses vs placebo (4.8 mEq/L, 4.5 mEq/L, and 4.4 mEq/L for 5 g, 10 g, and 15 g, respectively; 5.1 mEq/L for placebo; P < 0.001 for all comparisons).^[80]

The HARMONIZE trial also included patients with heart failure who were maintained on RAASi. Compared with placebo, all 3 zirconium cyclosilicate doses lowered potassium and effectively maintained normokalemia for 28 days in those patients, without the need to adjust RAASi regimens.^[81]

Peacock et al conducted a pilot evaluation of the efficacy for use of sodium zirconium cyclosilicate (SZC) with insulin and glucose for the treatment of hyperkalemia in the ED. In the phase II, multicenter, randomized, double-blind, placebo-controlled study 70 patients with blood potassium ≥ 5.8 mmol/L were randomized to receive SZC 10 g or placebo, up to three times during a 10-hour period, with insulin and glucose. A lower proportion of patients receiving SZC required additional potassium-lowering therapy at 0 to 4 hours compared to those receiving the placebo (15.6% vs. 30.6%, respectively; odds ratio = 0.40, 95% CI = 0.09 to 1.77).^[82]

Step 5

Emergency dialysis is a final recourse for patients who are experiencing potentially lethal hyperkalemia that has not responded to more conservative measures or for patients who have complete kidney failure. Initiation of dialysis can often take several hours; therefore, even if dialysis is contemplated, the other therapeutic modalities should be instituted as a bridge to dialysis.

The final step in the medical management of hyperkalemia is to determine the cause of hyperkalemia in order to prevent future episodes. This should include examination of the following:

Sources of potassium intake
Causes of decreased renal excretion
Causes of impaired cellular uptake

Surgical Therapy

Surgical intervention generally is not needed for the care of a patient with hyperkalemia. Patients with metabolic acidosis and consequent hyperkalemia due to ischemic gut obviously require exploration. Patients with hyperkalemia due to rhabdomyolysis may need surgical decompression of swollen, ischemic muscle compartments. Patients without end-stage kidney disease who require hemodialysis for control of hyperkalemia require placement of a hemodialysis catheter for emergency dialysis.^[83]

In patients with solid tumors, tumor debulking may be considered as a means of decreasing the risk of hyperkalemia from tumor lysis syndrome.^[84]

Complications of Treatment

Complications of therapy include the following:

Failure to control hyperkalemia
Hypokalemia due to excessively aggressive therapy
Hypercalcemia due to excessive calcium administration
Hypocalcemia from excessive bicarbonate therapy
Chest discomfort or tachycardia due to beta-agonist therapy
Hypoglycemia or hyperglycemia complicating glucose and insulin administration
Metabolic alkalosis and tetany due to excessive sodium bicarbonate administration
Volume depletion, metabolic alkalosis, kidney insufficiency, hypocalcemia, hypomagnesemia, and hypophosphatemia due to aggressive loop diuretic use
Colon perforation due to exchange resin administration

Treatment of pseudohyperkalemia may result in hypokalemia; thus, treatment of non–life-threatening hyperkalemia should be deferred pending verification of hyperkalemia.

Diet and Activity

A low-potassium diet containing 2 g of potassium is recommended so as to minimize potassium intake in patients at risk for hyperkalemia. In particular, potassium intake must be closely monitored (and possibly restricted) in patients with kidney failure.

No restrictions on activity are necessary unless continuous monitoring for cardiotoxicity is required.

Prevention

Inform patients at risk for hyperkalemia about dietary sources of potassium, including salt substitutes. Adjust the diet to decrease potassium dietary load. Adjust medications that predispose to or exacerbate hyperkalemia.

Renin-angiotensin-aldosterone system inhibitors

Although fears of hyperkalemia may be a barrier to use of renin-angiotensin-aldosterone system inhibitors (RAASis), RAASi therapy has been shown to improve survival among patients with chronic kidney disease (CKD), chronic heart failure (CHF), and diabetes.^[85]In a cohort study of patients who experienced a decline in estimated glomerular filtration rate (eGFR) to less than 30 mL/min/1.73 m² while receiving RAASi therapy, discontinuation of RAASi therapy was associated with a higher risk of mortality or major adverse cardiovascular events than continuation of therapy.^[86]

In a retrospective observational study of 27,355 patients with diabetes, Raebel et al concluded that potassium monitoring can reduce the incidence of serious hyperkalemia-associated adverse events in patients with diabetes and CKD who are receiving RAASi therapy. The investigators found that for monitored patients with diabetes alone, the adjusted relative risk for such events was 0.50, whereas for monitored patients who also had CKD, the adjusted relative risk was 0.29.^[17]

Concurrent use of multiple strategies to mitigate hyperkalemia is recommended for patients with CKD who are receiving RAASi therapy. These include the following^[87]

Discontinue non-RAASi medications that are known to cause hyperkalemia
Correct metabolic acidosis
Maximize medication therapies that lower serum potassium, including diuretics and sodium-glucose cotransporter-2 (SGLT-2) inhibitors (see below)
Consider initiation of potassium exchange resins

Mineralocorticoid receptor antagonists

Although spironolactone and eplerenone—first- and second-generation steroidal mineralocorticoid receptor antagonists (MRAs), respectively—are strongly recommended for patients with CKD and CHF, they are underutilized because of safety concerns including the potential development of hyperkalemia.^[88]

Finerenone, a third-generation non-steroidal MRA, is associated with a lower risk of hyperkalemia.^[88]A meta-analysis of randomized clinical trials found that risk for hyperkalemia was higher with finerenone than with with placebo, but only a small proportion of patients discontinued treatment due to hyperkalemia, and no deaths were attributed to hyperkalemia.^[89]A protocol of routine potassium monitoring with temporary treatment interruption and dose reduction was validated in two trials; the protocol decreased the risk of clinically significant hyperkalemia and thereby increased the safety of finerenone for patients with CKD and type 2 diabetes.^[90]

Sodium-glucose cotransporter 2 inhibitors

SGLT2 inhibitors reduce the risk of cardiorenal events in patients with type 2 diabetes who are at high cardiovascular risk or have CKD. A meta-analysis of 6 trials of 4 SGLT2 inhibitors, comprising 49,875 patients, concluded that SGLT2 inhibitors reduced the risk of serious hyperkalemia (hazard ratio, 0.84) without increasing the risk of hypokalemia.^[91]

Consultations

For patients with severe hyperkalemia or kidney failure, early consultation with a nephrologist for aid in implementing efficient therapy and plans for dialysis is highly recommended. In addition, these patients should be admitted to an intensive care unit (ICU).

Consultations with the following specialists may be necessary in cases of hyperkalemia that result from certain conditions or disease states:

Pediatric intensivist or neonatologist – For life-threatening hyperkalemia (hyperkalemia with ECG changes) in infants and children
Social services specialist – For hyperkalemia developing in children after unintentional ingestions or poisonings
Cardiologist - For emergency pacemaker placement in patients with refractory heart block
Hematologist/oncologist – For hyperkalemia resulting from tumor lysis syndrome
Nutritional support specialist - For hyperkalemia caused by kidney failure, which requires close regulation of potassium and sodium intake
Endocrinologist – For suspected mineralocorticoid abnormalities (eg, congenital adrenal hyperplasia)

Long-Term Monitoring

For patients whose hyperkalemia resulted from a single, clearly defined episode (eg, acute exertional rhabdomyolysis or drug-induced hemolysis), infrequent monitoring of serum potassium generally suffices. However, for patients who have conditions or medications that will continue to predispose to hyperkalemia, more frequent monitoring of serum potassium is required. For patients at high risk, monthly measurements are indicated.

Continuing care relates to the disease process that led to the hyperkalemia. For patients who have recurrent or constant hyperkalemia (eg, those with diabetic nephropathy and type IV renal tubular acidosis), long-term therapy with an oral loop diuretic and sodium polystyrene sulfonate (SPS) may be indicated. For pseudohypoaldosteronism type II, the treatment of choice is a thiazide diuretic.

Medication

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Media Gallery

Widened QRS complexes in patient whose serum potassium level was 7.8 mEq/L.
ECG of patient with pretreatment potassium level of 7.8 mEq/L and widened QRS complexes after receiving 1 ampule of calcium chloride. Note narrowing of QRS complexes and reduction of T waves.
Hyperkalemia diagnosis and treatment flow chart.
Widened QRS complexes in hyperkalemia.

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#author-disclosures{display:block}#author-disclosures.modal-layer{position:relative}#author-disclosures .modal-content{max-height:none}#author-disclosures .close-modal{display:none}

Author

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Society of Nephrology<br/>Received income in an amount equal to or greater than $250 from: Healthcare Quality Strategies, Inc.

Coauthor(s)

Zygimantas C Alsauskas, MD Assistant Professor of Medicine, Division of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

Zygimantas C Alsauskas, MD is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

Lina Mackelaite, MD Assistant Professor of Medicine, University of Louisville School of Medicine

Lina Mackelaite, MD is a member of the following medical societies: American Society of Hypertension, American Society of Nephrology, American Society of Transplantation, National Kidney Foundation

Disclosure: Nothing to disclose.

Vibha Nayak, MD Assistant Professor of Nephrology, Director of Home Dialysis, Kidney Disease Program, University of Louisville School of Medicine

Vibha Nayak, MD is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FASN Professor of Medicine, Section of Nephrology-Hypertension, Deming Department of Medicine, Tulane University School of Medicine

Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Acknowledgements

Son Dinh, MD Nephrologist, Southland Renal Medical Group, Inc

Son Dinh, MD is a member of the following medical societies: American Society of Nephrology and National Kidney Foundation

Disclosure: Nothing to disclose.

Anil Kumar Mandal, MD Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida School of Medicine

Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, and Central Society for Clinical Research

Disclosure: Nothing to disclose.

Rosemary Ouseph, MD Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine

Rosemary Ouseph, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society of Nephrology, and American Society of Transplant Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

Factor	Effect on Plasma K⁺	Mechanism
Aldosterone	Decrease	Increases sodium resorption, and increases K⁺ excretion
Insulin	Decrease	Stimulates K⁺ entry into cells by increasing sodium efflux (energy-dependent process)
Beta-adrenergic agents	Decrease	Increases skeletal muscle uptake of K⁺
Alpha-adrenergic agents	Increase	Impairs cellular K⁺ uptake
Acidosis (decreased pH)	Increase	Impairs cellular K⁺ uptake
Alkalosis (increased pH)	Decrease	Enhances cellular K⁺ uptake
Cell damage	Increase	Intracellular K⁺ release
Succinylcholine	Increase	Cell membrane depolarization

Hyperkalemia Treatment & Management

Approach Considerations

Initial Emergency Management

Pharmacologic Therapy and Dialysis

Step 1

Step 2

Step 3

Step 4

Step 5

Surgical Therapy

Complications of Treatment

Diet and Activity

Prevention

Renin-angiotensin-aldosterone system inhibitors

Mineralocorticoid receptor antagonists

Sodium-glucose cotransporter 2 inhibitors

Consultations

Long-Term Monitoring

References

Tables

Contributor Information and Disclosures

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