What is the treatment for hyperkalemia?

Treatment of Hyperkalemia (K+ 5.22 mEq/L)

For a potassium of 5.22 mEq/L (mild hyperkalemia), obtain an ECG immediately and if normal with no symptoms, focus on identifying and eliminating contributing medications (especially RAAS inhibitors, NSAIDs, potassium-sparing diuretics), optimizing diuretics if kidney function permits, and initiating a newer potassium binder (patiromer or sodium zirconium cyclosilicate) rather than discontinuing life-saving RAAS inhibitors. 1, 2, 3

Immediate Assessment

• Obtain an ECG immediately to check for peaked T waves, flattened P waves, prolonged PR interval, or widened QRS—these findings mandate emergency treatment regardless of the exact potassium value 1, 2
• Rule out pseudohyperkalemia from hemolysis, repeated fist clenching during blood draw, or delayed sample processing by repeating the measurement with proper technique 1, 2
• At 5.22 mEq/L without ECG changes, this is mild hyperkalemia and does not require emergency hospitalization or acute interventions like calcium, insulin, or albuterol 1, 2, 3

Identify and Address Root Causes

Medication Review (Most Critical Step)

Immediately review and adjust these medications: 1, 3

• RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists): Do NOT discontinue permanently—these provide mortality benefit in cardiovascular disease and slow CKD progression. Instead, consider temporary dose reduction if K+ rises above 6.0 mEq/L 1, 2, 4
• NSAIDs: Discontinue unless absolutely essential—they impair renal potassium excretion 1, 3
• Potassium-sparing diuretics (spironolactone, amiloride, triamterene): Hold temporarily 1, 3
• Other contributors: Trimethoprim, heparin, beta-blockers, calcineurin inhibitors 1, 3
• Dietary sources: Eliminate potassium supplements and "low-salt" substitutes (high in potassium) 1, 3

Assess Risk Factors

Patients at highest risk for recurrent hyperkalemia include those with: 1, 2, 3

• Chronic kidney disease (prevalence up to 73% in advanced CKD)
• Heart failure (prevalence up to 40%)
• Diabetes mellitus
• Concurrent use of multiple RAAS inhibitors

Treatment Algorithm for K+ 5.22 mEq/L

Step 1: Optimize Diuretic Therapy

• Initiate or increase loop diuretics (furosemide 40-80 mg daily) if adequate kidney function (eGFR >30 mL/min) to increase urinary potassium excretion 1, 3
• Thiazide diuretics are an alternative if eGFR >30 mL/min 1
• Titrate diuretics to maintain euvolemia, not primarily for potassium management 1

Step 2: Initiate Potassium Binder Therapy

Newer potassium binders are strongly preferred over sodium polystyrene sulfonate (Kayexalate), which carries risk of bowel necrosis and has limited efficacy: 1, 2, 3

First-Line: Sodium Zirconium Cyclosilicate (SZC/Lokelma)

• Dosing: 10 g three times daily for 48 hours, then 5-15 g once daily for maintenance 1, 3
• Onset: Approximately 1 hour—fastest acting binder 1, 3
• Mechanism: Highly selective potassium binding, exchanging hydrogen and sodium for potassium 1
• Monitoring: Watch for edema due to sodium content 1

Alternative: Patiromer (Veltassa)

• Dosing: Start 8.4 g once daily with food, titrate up to 25.2 g daily based on potassium response 1, 3
• Onset: Approximately 7 hours 1, 3
• Mechanism: Exchanges calcium for potassium in the colon 1
• Critical caveat: Separate from other oral medications by at least 3 hours 1, 3
• Monitoring: Check magnesium levels—patiromer causes hypomagnesemia (for each 1 mEq/L increase in magnesium, potassium increases by 1.07 mEq/L) 1

Step 3: Maintain RAAS Inhibitor Therapy

This is the most important principle in chronic hyperkalemia management: 1, 2, 4

• Do NOT permanently discontinue RAAS inhibitors in patients with heart failure, proteinuric CKD, or cardiovascular disease—these drugs provide mortality benefit and slow disease progression 1, 2, 4
• Use potassium binders to enable continuation of life-saving RAAS inhibitor therapy 1, 2, 3
• Only temporarily reduce or hold RAAS inhibitors if K+ exceeds 6.5 mEq/L, then restart at lower dose once K+ <5.0 mEq/L with concurrent binder therapy 1, 2

Monitoring Protocol

• Check potassium within 1 week of starting potassium binder or adjusting RAAS inhibitor doses 1, 3
• Reassess potassium 7-10 days after initiating binder therapy 1, 3
• For patients on RAAS inhibitors, check potassium and renal function at 1-2 weeks, 3 months, then every 6 months 1
• High-risk patients (CKD, diabetes, heart failure, history of hyperkalemia) require more frequent monitoring 1, 2, 3

Dietary Considerations

Evidence linking dietary potassium intake to serum potassium is limited, and stringent dietary restrictions may not be necessary, especially in patients on potassium binders: 1, 4

• Potassium-rich diets provide cardiovascular benefits including blood pressure reduction 1, 3
• Focus on reducing nonplant sources of potassium rather than blanket restriction 4
• Newer potassium binders may allow less restrictive dietary potassium intake 1

Critical Pitfalls to Avoid

• Do NOT discontinue RAAS inhibitors prematurely—this leads to worse cardiovascular and renal outcomes. Use dose reduction plus potassium binders instead 1, 2, 4
• Do NOT use sodium polystyrene sulfonate (Kayexalate)—it has delayed onset, limited efficacy, and risk of bowel necrosis. Use newer binders (patiromer or SZC) 1, 2, 3
• Do NOT delay treatment while waiting for repeat lab confirmation if clinical suspicion is high 2
• Do NOT rely solely on dietary restriction—medication adjustment and binder therapy are more effective 1, 4
• Do NOT forget to monitor magnesium in patients on patiromer—hypomagnesemia can paradoxically worsen hyperkalemia 1

When to Escalate Care

Urgent hospitalization and emergency treatment are required if: 1, 2

• Any ECG changes present (peaked T waves, widened QRS, prolonged PR, arrhythmias)
• Potassium >6.5 mEq/L
• Rapid rise in potassium level
• Symptomatic hyperkalemia (muscle weakness, paresthesias, palpitations)