Acute management of hyperkalemia involves various interventions, including the intravenous administration of calcium salts or drugs that affect the cellular distribution of K+, and definitive measures to remove K+ from the body. The effects of interventions that alter the distribution of K+ usually occur within a short period of time (<1h), but they do not affect total body K+ levels. Definitive therapy for hyperkalemia in patients with a net positive K+ balance necessitates the removal of K+ from the body.

Explore below to learn more about the different treatments for hyperkalemia.


Calcium gluconate

Treatment of Hyperkalemia: Calcium gloconate. Onset of Action: 1-3 minutes. Advantages: Efficacy can be monitored with ECG. Dose can be repeated if no changes observed. Limitations: Does not reduce total K+ levels. Short duration of effect (30-60 minutes). Risk of hypoglycemia. Avoid in patients receiving digoxin.

Calcium gluconate, administered parenterally, has the fastest onset of action among drugs used for the treatment of hyperkalemia and is used when ECG changes are present. It is administered to stabilize the myocardium; it lowers the threshold potential, thus counteracting the toxic effect of high K+.


Treatment of Hyperkalemia: Insulin/Glucose. Onset of Action: 30 minutes. Advantages: Effects last 4-6 hours. Limitations: Does not reduce total K+ levels and Risk of hypoglycemia.

Intravenous administration of 10 units of regular insulin with 50 g of glucose can help prevent hypoglycemia

β2 receptor agonists

Treatment of Hyperkalemia: Beta 2 receptor agonists. Onset of Action: approximately 30 minutes. Advantages: Effect is independent of insulin and aldosterone. Limitations: Does not reduce total K+ levels. Short duration with inconsistent effect (2-4 hours). Use with caution in ischemic heart disease (risk of tachycardia)

β2 agonists can be administered intravenously, subcutaneously, or inhaled. They work by redistributing K+ to the intracellular space. The effect of β2 agonists is additive to that of insulin administration and they can be taken together. It should be noted that β2 agonists may be ineffective in up to 25% of patients when given by a nebulizer.


Sodium bicarbonate

Treatment of Hyperkalemia: Sodium bicarbonate. Onset of Action: Effects may be observed after 4-6 hours. Advantages: Recommended when metabolic acidosis is the cause of hyperkalemia. Limitations: Risk of metabolic alkalosis. Risk of volume overload. Risk of large sodium load.

Sodium bicarbonate facilitates the movement of K+ from the plasma into the cell. However, due to the fact that sodium bicarbonate does not lower K+ in the absence of metabolic acidosis, experts no longer recommend this treatment except in patients with severe metabolic acidosis. In addition, this treatment generates a large sodium load, often a major factor limiting its use in patients with heart failure.


Treatment of Hyperkalemia: Diuretics. Onset of Action: Depends on the start of diuresis. Advantages: Beneficial in patients with volume expansion. Limitations: Efficacy depends on residual renal function (until diuresis is present). Are non-selective and therefore affect many electrolytes.  May produce volume depletion. May reduce K+ excretion.  May produce decreased distal nephron flow. May produce additional electrolyte disturbances. May lead to worsening of kidney function. Increased risk of gout and diabetes.

Loop or thiazide diuretics are sometimes used to prevent a rise in serum K+ by increasing the distal delivery of sodium and urine flow rate, effects that promote a kaliuresis.

According to KDOQI guidelines, thiazide diuretics given once daily are recommended in patients with GFR ≥30 mL/min/1.73 m2 (CKD stage 1-3), while loop diuretics given once or twice daily are recommended in patients with GFR <30 mL/min/1.73 m2 (CKD stage 4-5). However, it should be noted that, in general, patients with decreased kidney function may be relatively resistant to the effects of diuretics.

Diuretics have been associated with a number of adverse reactions. KDOQI guidelines recommend that patients being treated with diuretics should be monitored for volume depletion (for which heart failure patients are especially at risk), hypokalemia, and other electrolyte disorders (like hypomagnesemia and hyponatremia, which can cause lasting damage).

Furthermore, use of diuretics in some patients may be a risk because some complications that arise from their use are rare or idiosyncratic; their occurrence cannot be anticipated or prevented.


Treatment of Hyperkalemia: Hemodialysis. Onset of Action: Within minutes. Advantages: Effects last until end of dialysis or longer. Limitations: Concentration of K+ in dialysate can contribute to hyperkalemia. Limitations and complications inherent to each dialysis modality (eg, arrhythmias with hemodialysis)

For patients who have persistent or severe hyperkalemia but very poor kidney function, such as stage 4 or 5 CKD, acute hemodialysis is the last course of action.

During hemodialysis, plasma K+ falls rapidly in the first hour and very little thereafter. If a 0-K dialysate is used, serum K+ may decrease by as much as 1.2 to 1.5 mEq/h. K+ concentrations show a rebound after dialysis is finished, and this rebound may require several hours to reach a plateau.

Sodium Polystyrene Sulfonate (SPS)

Treatment of Hyperkalemia: Sodium Polystyrene Sulfonate (SPS). Onset of Action: 2 hours. Advantages: Effects may last 4-6 hours or longer depending on ongoing K+ intake or cellular redistribution. Limitations: No controlled long-term data. Serious GI adverse events reported, including fatal cases of intestinal necrosis. caution with sodium loads in patients with congestive heart failure, hypertension, or edema.

GI excretion is accomplished using SPS, which binds K+ in the colon in exchange for sodium. Experimental studies suggest that the sorbitol added to sodium polystyrene sulphonate is the main exacerbating factor for colonic necrosis. However, some case reports suggest that polystyrene sulphonate derivatives administered without sorbitol can also cause gastrointestinal toxicity.

MAINTENANCE Treatments1,4,11

Low K+ diet

Treatment of Hyperkalemia: Low K+ diet. Advantages: May improve metabolic acidosis. Limitations: Adherence is difficult. Limiting K+-rich foods can cause constipation. Contradicts the DASH diet, may worsen chronic hypertension.

The National Kidney Disease Education Program supports dietary restriction of K+ for initial management of hyperkalemia in patients with CKD. While this strategy helps limit intake, it does not address any underlying kidney dysfunction that is reducing the excretion of K+.

This table lists foods high in potassium. Topping the list is the avocado, which has approximately 38 milliequivalents of potassium. Bananas, reputed to be among the foods highest in potassium, have comparatively less potassium content, just 12 milliequivalents.

Reproduced with permission from Weiner ID, Linas SL, Wingo CS. Disorders of Potassium Metabolism. In: Johnson R, Fluege J, Feehally J, eds. Comprehensive Clinical Nephrology. 4th ed. Philadelphia, PA: Saunders Elsevier; 2010:118-129.

Visit the organizations below for more information on K+-rich foods and strategies to establish a better dietary routine.

Discontinuation/dose reduction of RAASi

Treatment of Hyperkalemia: Discontinuation/dose reduction of RAASi. Advantages: Prevention of recurrent hyperkalemic events. Limitations: Stopping or suboptimal utilization of renal/cardioprotective RAASi therapy.

The most vexing clinical problem is the management of hyperkalemia in patients receiving RAAS inhibitors, as the known beneficial effects of these agents on both kidney function and cardiovascular disease makes their discontinuation undesirable. Nonetheless, discontinuation rates of these agents remain very high in patients with CKD.