What is the initial management of hyperkalemia in a patient under the care of a nephrologist?

Hyperkalemia Workup by Nephrologist

For a nephrologist managing hyperkalemia, the workup should immediately focus on severity classification, ECG assessment, and identifying reversible causes—particularly medication review and renal function evaluation—while simultaneously initiating appropriate treatment based on potassium level and cardiac manifestations. 1

Initial Assessment and Classification

Severity Stratification

• Mild hyperkalemia: 5.0-5.9 mEq/L 2, 1
• Moderate hyperkalemia: 6.0-6.4 mEq/L 2, 1
• Severe hyperkalemia: ≥6.5 mEq/L (life-threatening) 2, 1

Immediate Diagnostic Steps

Rule out pseudohyperkalemia first by repeating measurement with proper blood sampling technique, as hemolysis or tissue breakdown during phlebotomy can falsely elevate potassium levels 1, 3. This is critical before initiating aggressive treatment.

Obtain ECG immediately regardless of potassium level, as ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent treatment need independent of the absolute potassium value 2, 1, 3.

Essential Laboratory Workup

• Complete metabolic panel: serum electrolytes, BUN, creatinine, glucose 1
• Complete blood count 1
• Urinalysis 1
• Assess kidney function: eGFR to determine renal potassium excretion capacity 1, 3
• Arterial blood gas if metabolic acidosis suspected (sodium bicarbonate only effective with concurrent acidosis) 2, 1

Medication Review (Critical Priority)

Immediately review and adjust these medications as they are the most common reversible causes 1, 3:

High-Priority Medications to Evaluate

• RAAS inhibitors: ACE inhibitors, ARBs, mineralocorticoid receptor antagonists (MRAs) 2, 1, 3
• Potassium-sparing diuretics: spironolactone, amiloride, triamterene 1, 3
• NSAIDs (attenuate diuretic effects and impair renal potassium excretion) 1, 3
• Other contributors: trimethoprim, heparin, beta-blockers 1, 3
• Supplements: potassium supplements, salt substitutes 1, 3

Critical caveat: Do not permanently discontinue RAAS inhibitors in patients with cardiovascular disease, heart failure, or proteinuric CKD, as these provide mortality benefit 1, 3. Instead, use dose reduction plus potassium binders 1.

Risk Factor Assessment

High-Risk Comorbidities Requiring Closer Monitoring

• Chronic kidney disease (especially stage 3-5) 1, 3
• Diabetes mellitus 1, 3
• Heart failure 1, 3
• History of recurrent hyperkalemia 1

Underlying Causes to Investigate

• Acute kidney injury or worsening CKD 1
• Metabolic acidosis (check pH, bicarbonate) 2, 1
• Tissue destruction: rhabdomyolysis, tumor lysis syndrome 1
• Endocrine disorders: adrenal insufficiency 3
• Inadequate dialysis in dialysis-dependent patients 3
• Constipation (reduces GI potassium excretion) 3

Treatment Algorithm Based on Severity

Severe Hyperkalemia (≥6.5 mEq/L) or Any ECG Changes

This is a medical emergency requiring immediate treatment 2, 1, 3:

Step 1: Cardiac Membrane Stabilization (immediate, within 1-3 minutes)

• Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes 2, 1
• Alternative: Calcium chloride 10%: 5-10 mL IV over 2-5 minutes (preferred if central access available) 2, 1
• Effect: Protects against arrhythmias but does NOT lower potassium; lasts only 30-60 minutes 2, 1
• Repeat dose if no ECG improvement within 5-10 minutes 1

Step 2: Shift Potassium into Cells (onset 15-30 minutes, lasts 4-6 hours)

• Insulin + glucose: 10 units regular insulin IV with 25g glucose (50 mL D50W) over 15-30 minutes 2, 1
• Nebulized albuterol: 10-20 mg over 15 minutes 2, 1
• Sodium bicarbonate: 50 mEq IV over 5 minutes ONLY if metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L) 2, 1

Step 3: Eliminate Potassium from Body

• Loop diuretics: furosemide 40-80 mg IV (only if adequate renal function) 2, 1
• Hemodialysis: most effective method for severe hyperkalemia, especially with renal failure 2, 1, 3
• Newer potassium binders: sodium zirconium cyclosilicate (SZC) or patiromer for ongoing management 2, 1

Medication adjustment: Temporarily discontinue or reduce RAAS inhibitors at K+ ≥6.5 mEq/L 2, 1

Moderate Hyperkalemia (6.0-6.4 mEq/L) Without ECG Changes

• If ECG changes present: treat as severe hyperkalemia 1
• If no ECG changes: initiate potassium-shifting therapies (insulin/glucose, albuterol) 1
• Loop diuretics if adequate renal function 1
• Consider potassium binders for ongoing management 1
• Reduce RAAS inhibitor dose by 50% rather than complete discontinuation 1

Mild Hyperkalemia (5.0-5.9 mEq/L)

• Do NOT initiate acute interventions (calcium, insulin, albuterol) unless ECG changes or symptoms present 1
• Review and adjust contributing medications 1, 3
• Dietary potassium restriction: <3 g/day (avoid bananas, oranges, potatoes, tomatoes, salt substitutes) 3
• Loop diuretics if adequate renal function 1
• For patients on RAAS inhibitors with K+ >5.0 mEq/L: initiate potassium binder (patiromer or SZC) while maintaining RAAS inhibitor therapy 2, 1

Chronic Management Strategy

For Patients Requiring RAAS Inhibitors

Maintain RAAS inhibitors using potassium binders rather than discontinuing these life-saving medications 2, 1, 3:

• Potassium 5.0-6.5 mEq/L: Initiate patiromer or SZC, maintain RAAS inhibitor 2, 1
• Potassium >6.5 mEq/L: Temporarily reduce/hold RAAS inhibitor, initiate potassium binder, restart at lower dose once K+ <5.0 mEq/L 2, 1

Potassium Binder Options

Sodium zirconium cyclosilicate (SZC/Lokelma) 1, 4:

• Initial treatment: 10 g three times daily for up to 48 hours 4
• Maintenance: 10 g once daily, adjust by 5 g increments based on potassium levels 4
• Onset: ~1 hour (faster than patiromer) 1
• Hemodialysis patients: 5 g once daily on non-dialysis days (10 g if K+ >6.5 mEq/L) 4

Patiromer (Veltassa) 1:

• Starting dose: 8.4 g once daily with food 1
• Titration: up to 25.2 g daily based on potassium response 1
• Onset: ~7 hours 1
• Separate from other medications by 3 hours 1
• Monitor magnesium levels (can cause hypomagnesemia) 1

Avoid sodium polystyrene sulfonate (Kayexalate) due to delayed onset, limited efficacy, and risk of bowel necrosis 2, 1

Monitoring Protocol

Acute Phase

• Check potassium every 2-4 hours after initial emergency interventions 1
• Continuous cardiac monitoring during calcium administration 1
• Monitor glucose to prevent hypoglycemia after insulin administration 2, 1

Chronic Management

• Check potassium within 1 week of starting or escalating RAAS inhibitors 1
• Reassess 7-10 days after initiating potassium binder therapy 1
• High-risk patients (CKD, diabetes, heart failure, history of hyperkalemia) require more frequent monitoring 1, 3
• Optimal target range: 4.0-5.0 mEq/L minimizes mortality risk 1
• Advanced CKD (stage 4-5): broader acceptable range of 3.3-5.5 mEq/L 1

Critical Pitfalls to Avoid

• Never delay treatment while waiting for repeat labs if ECG changes present 1, 3
• Never use sodium bicarbonate without metabolic acidosis—it is ineffective and wastes time 2, 1
• Never give insulin without glucose—hypoglycemia can be life-threatening 1
• Never rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
• Remember calcium, insulin, and beta-agonists are temporizing only—they do NOT remove potassium from the body 2, 1
• Do not permanently discontinue RAAS inhibitors in cardiovascular disease or proteinuric CKD—use dose reduction plus potassium binders instead 2, 1, 3
• Rebound hyperkalemia occurs 2-4 hours after temporary measures wear off—must initiate definitive potassium removal strategies 2, 1

Indications for Hospital Admission

• Potassium >6.0 mEq/L regardless of symptoms 3
• Any ECG changes (peaked T waves, widened QRS, prolonged PR, arrhythmias) 3
• Symptomatic hyperkalemia (muscle weakness, paresthesias) 3
• High-risk comorbidities: advanced CKD, heart failure, diabetes 3
• Rapid deterioration of kidney function 3