How should hyperkalaemia be treated in primary care?

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Last updated: February 11, 2026View editorial policy

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How to Treat Hyperkalemia in Primary Care

In primary care, mild-to-moderate hyperkalemia (5.0–6.4 mEq/L) without ECG changes should be managed by eliminating contributing medications (NSAIDs, potassium supplements, salt substitutes), optimizing diuretics if renal function permits, and initiating newer potassium binders (patiromer or sodium zirconium cyclosilicate) while maintaining life-saving RAAS inhibitors rather than discontinuing them. 1


Immediate Assessment: Determine Severity and Need for Hospital Transfer

Classification of Hyperkalemia

  • Mild: 5.0–5.9 mEq/L 1
  • Moderate: 6.0–6.4 mEq/L 1
  • Severe: ≥6.5 mEq/L 1

Obtain an ECG Immediately

  • ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent treatment regardless of potassium level and mandate immediate hospital transfer 1, 2
  • ECG findings can be highly variable and less sensitive than laboratory tests, so do not rely solely on ECG—a normal ECG does not exclude the need for treatment 1

Indications for Immediate Hospital Referral

  • Potassium >6.0 mEq/L regardless of symptoms 2
  • Any ECG changes suggestive of hyperkalemia 2
  • Symptomatic hyperkalemia (muscle weakness, paresthesias, palpitations) 2
  • High-risk comorbidities: advanced CKD, heart failure, diabetes mellitus 2
  • Rapid rise in potassium or ongoing potassium release (tumor lysis syndrome, rhabdomyolysis) 1

Outpatient Management of Mild-to-Moderate Hyperkalemia (5.0–6.4 mEq/L, No ECG Changes)

Step 1: Rule Out Pseudohyperkalemia

  • Repeat the measurement with proper technique (avoid fist clenching, hemolysis, prolonged tourniquet time) or use arterial sampling to exclude laboratory artifact 1

Step 2: Eliminate Contributing Factors

Medications to Stop or Reduce

  • NSAIDs: Attenuate diuretic effects and impair renal potassium excretion 1
  • Potassium supplements and salt substitutes: Eliminate immediately 1, 2
  • Trimethoprim, heparin, beta-blockers: Review and discontinue if possible 1
  • Potassium-sparing diuretics (amiloride, triamterene): Hold temporarily 1

RAAS Inhibitors (ACE Inhibitors, ARBs, Mineralocorticoid Receptor Antagonists)

  • Do NOT permanently discontinue RAAS inhibitors in patients with cardiovascular disease, heart failure, or proteinuric CKD—these medications provide mortality benefit 1, 2
  • For potassium 5.0–6.5 mEq/L: Initiate a potassium-lowering agent (patiromer or sodium zirconium cyclosilicate) and maintain RAAS inhibitor therapy unless an alternative treatable cause is identified 1
  • For potassium >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitor dose, initiate a potassium-lowering agent, and restart RAAS inhibitor at a lower dose once potassium <5.0 mEq/L 1

Step 3: Optimize Diuretic Therapy (If Adequate Renal Function)

  • Loop diuretics (furosemide 40–80 mg daily) increase urinary potassium excretion when eGFR >30 mL/min and urine output is adequate 1
  • Titrate diuretics to maintain euvolemia, not primarily for potassium management 1

Step 4: Initiate Potassium Binders

Preferred Agents (NOT Sodium Polystyrene Sulfonate)

  • Sodium polystyrene sulfonate (Kayexalate) has significant limitations: delayed onset of action, risk of bowel necrosis, and lack of efficacy data—avoid for acute management 1, 3

Patiromer (Veltassa)

  • Starting dose: 8.4 g once daily with food 1
  • Titration: Increase to 16.8 g or 25.2 g daily based on potassium response 1
  • Onset of action: ~7 hours 1
  • Administration: Separate from other oral medications by at least 3 hours to avoid reduced absorption 1
  • Monitoring: Check potassium and renal function within 1 week of starting or adjusting dose 1

Sodium Zirconium Cyclosilicate (SZC/Lokelma)

  • Starting dose: 10 g three times daily for 48 hours, then 5–15 g once daily for maintenance 1
  • Onset of action: ~1 hour (suitable for more urgent outpatient scenarios) 1
  • Monitoring: Check potassium within 1 week of starting therapy 1

Step 5: Dietary Counseling

  • Limit high-potassium foods: Bananas, oranges, potatoes, tomatoes, legumes, chocolate, yogurt 2
  • Avoid salt substitutes containing potassium 1
  • Avoid herbal supplements: Alfalfa, dandelion, horsetail, nettle 1
  • Note: Evidence linking dietary potassium intake to serum levels is limited, and a potassium-rich diet has cardiovascular benefits—stringent restriction may not be necessary in patients receiving potassium binder therapy 1

Monitoring Protocol

Initial Monitoring

  • Check potassium and renal function within 7–10 days after starting or increasing RAAS inhibitors 1
  • Recheck potassium within 1 week after initiating potassium binder therapy 1

Ongoing Monitoring

  • Individualize frequency based on eGFR, heart failure, diabetes, or history of hyperkalemia 1
  • High-risk patients (CKD, diabetes, heart failure, RAAS inhibitor use) require more frequent monitoring 1
  • Target potassium range: 4.0–5.0 mEq/L to minimize mortality risk 1

Special Populations

Patients with CKD

  • Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders, as these drugs slow CKD progression 1
  • Optimal potassium range is broader in advanced CKD: 3.3–5.5 mEq/L for stage 4–5 CKD versus 3.5–5.0 mEq/L for stage 1–2 CKD 1

Patients with Heart Failure

  • Do NOT discontinue RAAS inhibitors or mineralocorticoid receptor antagonists due to hyperkalemia—use potassium binders to maintain these life-saving medications 1
  • For potassium >5.5 mEq/L: Reduce mineralocorticoid receptor antagonist dose by 50% (e.g., spironolactone 25 mg to 12.5 mg) 2

Critical Pitfalls to Avoid

Do NOT Delay Treatment While Awaiting Repeat Labs

  • If ECG changes are present, do NOT delay treatment while waiting for repeat potassium levels—ECG changes indicate urgent need regardless of the exact potassium value 1

Do NOT Rely Solely on ECG Findings

  • ECG changes are highly variable and less sensitive than laboratory tests 1

Do NOT Permanently Discontinue RAAS Inhibitors

  • Discontinuing RAAS inhibitors leads to worse cardiovascular and renal outcomes 1, 2
  • Dose reduction plus potassium binders is preferred to maintain mortality and morbidity benefits 2

Do NOT Use Sodium Bicarbonate Without Metabolic Acidosis

  • Sodium bicarbonate is only indicated when metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L)—it is ineffective without acidosis 1

Do NOT Ignore Magnesium Levels

  • Hypomagnesemia can make hyperkalemia resistant to correction 1

When to Escalate Care

Immediate Hospital Referral Indicated If:

  • Potassium rises above 6.0 mEq/L on repeat testing 2
  • ECG changes develop (peaked T waves, widened QRS, prolonged PR interval) 2
  • Patient develops symptoms (muscle weakness, paresthesias, palpitations) 2
  • Rapid deterioration of renal function occurs 2

Team Approach

  • Optimal management involves specialists (cardiologists, nephrologists), primary care physicians, nurses, pharmacists, social workers, and dietitians 1
  • Educational initiatives on newer potassium binders are needed to improve chronic hyperkalemia management 1

References

Guideline

Hyperkalemia Management Guidelines

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Guideline

Hyperkalemia Management Guidelines

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

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Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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