How do you manage hyperkalemia in patients with chronic kidney disease (CKD) and impaired renal function?

Hyperkalemia Management in Chronic Kidney Disease

Immediate Assessment and Risk Stratification

In patients with CKD and hyperkalemia, immediately obtain an ECG and classify severity: mild (5.0-5.9 mEq/L), moderate (6.0-6.4 mEq/L), or severe (≥6.5 mEq/L), with ECG changes indicating urgent treatment regardless of potassium level. 1

• Verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating treatment 1
• Look for peaked T waves, flattened P waves, prolonged PR interval, and widened QRS complexes on ECG, though these findings can be highly variable and less sensitive than laboratory values 1
• Assess renal function (eGFR) and identify contributing factors: medications (ACE inhibitors, ARBs, MRAs, NSAIDs, potassium-sparing diuretics), dietary potassium intake, and concurrent metabolic acidosis 1, 2

Acute Management of Severe Hyperkalemia (K+ ≥6.5 mEq/L or ECG Changes)

Administer IV calcium gluconate first to protect against arrhythmias within 1-3 minutes, as calcium does NOT lower potassium—it only stabilizes the cardiac membrane temporarily for 30-60 minutes. 1

Cardiac Membrane Stabilization

• Give calcium gluconate 10%: 15-30 mL IV over 2-5 minutes, or calcium chloride 10%: 5-10 mL IV over 2-5 minutes 1, 2
• Monitor ECG continuously during and for 5-10 minutes after administration 1
• If no ECG improvement within 5-10 minutes, repeat the dose 1
• Never delay calcium administration while waiting for repeat lab confirmation if ECG changes are present 1

Intracellular Potassium Shift (Administer All Three Agents Together)

• Insulin 10 units regular IV + 25g dextrose (D50W 50 mL): lowers potassium by 0.5-1.2 mEq/L within 30-60 minutes, effects last 4-6 hours 1, 2
• Nebulized albuterol 10-20 mg in 4 mL: lowers potassium by 0.5-1.0 mEq/L within 30-60 minutes, effects last 2-4 hours 1
• Sodium bicarbonate 50 mEq IV over 5 minutes: ONLY if metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L), as it is ineffective without acidosis 1, 2

Potassium Removal from the Body

• Loop diuretics (furosemide 40-80 mg IV): increase renal potassium excretion if adequate kidney function exists (eGFR >30 mL/min) 1
• Hemodialysis: the most effective and reliable method for severe hyperkalemia, especially in patients with oliguria, ESRD, or unresponsive to medical management 1, 2
• Avoid sodium polystyrene sulfonate (Kayexalate): significant limitations including delayed onset of action and risk of bowel necrosis 1

Monitoring Protocol

• Recheck potassium within 1-2 hours after insulin/glucose administration 1
• Continue monitoring every 2-4 hours during the acute treatment phase until stabilized 1
• Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 1

Management of Moderate Hyperkalemia (K+ 6.0-6.4 mEq/L, No ECG Changes)

For moderate hyperkalemia without ECG changes, initiate intracellular shift agents (insulin/glucose and albuterol) and begin potassium removal strategies while addressing underlying causes. 1

• Administer insulin 10 units IV + 25g dextrose and nebulized albuterol 10-20 mg as described above 1
• Initiate loop diuretics if adequate renal function present 1
• Start newer potassium binders (patiromer or sodium zirconium cyclosilicate) for sustained potassium control 1, 3, 4
• Temporarily hold or reduce RAAS inhibitors until potassium <5.0 mEq/L 1

Chronic Hyperkalemia Management (K+ 5.0-6.5 mEq/L)

The priority in chronic hyperkalemia management is maintaining life-saving RAAS inhibitor therapy using newer potassium binders rather than discontinuing these medications that provide mortality benefit in CKD. 5, 1

Medication Review and Adjustment

• Do NOT permanently discontinue RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) in patients with CKD, as these drugs slow CKD progression and improve cardiovascular outcomes 5, 1
• Review and eliminate contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 1
• For K+ 5.0-6.5 mEq/L on RAAS inhibitors: initiate approved potassium-lowering agent and maintain RAAS inhibitor therapy unless alternative treatable etiology identified 1
• For K+ >6.5 mEq/L: temporarily discontinue or reduce RAAS inhibitor, initiate potassium-lowering agent when K+ >5.0 mEq/L 1

Newer Potassium Binders (First-Line for Chronic Management)

Patiromer (Veltassa) and sodium zirconium cyclosilicate (SZC/Lokelma) are now preferred over sodium polystyrene sulfonate for long-term management, allowing continuation of life-saving RAAS inhibitor therapy. 1, 3, 4

Patiromer (Veltassa) 3

• Starting dose: 8.4 g once daily with food
• Titration: increase by 8.4 g increments weekly based on potassium levels, up to maximum 25.2 g daily
• Onset of action: ~7 hours
• Mechanism: binds potassium in exchange for calcium in the colon, increasing fecal excretion
• Administration: separate from other oral medications by at least 3 hours (except amlodipine, cinacalcet, clopidogrel, furosemide, lithium, metoprolol, trimethoprim, verapamil, warfarin which do not require separation) 3
• Monitoring: check potassium within 1 week of starting or dose adjustment, then monthly for 3 months, then every 3-6 months 1
• Side effects: hypomagnesemia (monitor magnesium levels), constipation 1

Sodium Zirconium Cyclosilicate (Lokelma) 4

• Acute phase: 10 g three times daily for 48 hours
• Maintenance: 5-15 g once daily
• Onset of action: ~1 hour (suitable for more urgent scenarios)
• Mechanism: exchanges hydrogen and sodium for potassium
• Administration: can be taken with or without food, separate other oral medications by at least 2 hours 4
• Monitoring: check potassium within 1 week, then monthly for 3 months, then every 3-6 months 1
• Side effects: edema (contains ~400 mg sodium per 5 g dose), hypokalemia 4
• Caution: avoid in patients with severe constipation, bowel obstruction, or impaction 4

Dietary Management

Implement an individualized approach that includes dietary interventions through a renal dietitian, limiting foods rich in bioavailable potassium (especially processed foods) while maintaining adequate nutrition. 5

• Limit high-potassium foods: processed foods, salt substitutes, bananas, oranges, potatoes, tomatoes 5, 1
• Avoid herbal supplements that raise potassium: alfalfa, dandelion, horsetail, nettle 1
• Evidence linking dietary potassium intake to serum levels is limited, and potassium-rich diets provide cardiovascular benefits including blood pressure reduction 1
• Stringent dietary restrictions may not be necessary in patients receiving potassium binder therapy 1

Diuretic Therapy

• Loop or thiazide diuretics promote urinary potassium excretion by stimulating flow to renal collecting ducts 1
• Furosemide 40-80 mg daily can be used if adequate renal function present (eGFR >30 mL/min) 1
• Titrate to maintain euvolemia, not primarily for potassium management 1

Special Considerations for Advanced CKD (Stages 4-5)

Patients with advanced CKD tolerate higher potassium levels due to compensatory mechanisms, but maintaining target potassium 4.0-5.0 mEq/L minimizes mortality risk. 1, 2

• 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
• Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders, as these drugs slow CKD progression 1
• Consider SGLT2 inhibitors to reduce hyperkalemia risk while providing renoprotection 5
• Individualize monitoring frequency based on CKD stage, heart failure, diabetes, or history of hyperkalemia 1, 2

Monitoring Protocol for CKD Patients on RAAS Inhibitors

Check potassium within 1 week of starting or escalating RAAS inhibitors, with reassessment 7-10 days after dose changes, especially in high-risk patients with CKD, heart failure, or diabetes. 1

Initial Monitoring

• Check potassium and renal function within 7-10 days after starting or increasing RAAS inhibitors 1
• Recheck at 1-2 weeks, 3 months, then every 6 months 1
• More frequent monitoring required in patients with eGFR <45 mL/min, heart failure, diabetes, or history of hyperkalemia 1

Ongoing Monitoring on Potassium Binders

• Check potassium within 1 week of starting potassium binder therapy 1
• Monitor weekly during dose titration phase 1
• Once stable: check at 1-2 weeks, 3 months, then every 6 months 1
• Critical: monitor closely not only for efficacy but also to protect against hypokalemia, which may be even more dangerous than hyperkalemia 1

Algorithm for RAAS Inhibitor Management Based on Potassium Levels

K+ 4.5-5.0 mEq/L (not on maximal RAAS inhibitor therapy):

• Initiate or up-titrate RAAS inhibitor therapy 1
• Monitor K+ closely 1

K+ >5.0-<6.5 mEq/L (on RAAS inhibitors):

• Initiate approved potassium-lowering agent (patiromer or SZC) 1
• Maintain RAAS inhibitor therapy unless alternative treatable etiology identified 1
• Consider adjustments to diet or concomitant medications to mitigate hyperkalemia 5

K+ >6.5 mEq/L:

• Discontinue or reduce RAAS inhibitor immediately 1
• Initiate potassium-lowering agent when K+ >5.0 mEq/L 1
• Restart RAAS inhibitor at lower dose once K+ <5.0 mEq/L with concurrent potassium binder therapy 1

Critical Pitfalls to Avoid

• Never delay treatment while waiting for repeat lab confirmation if ECG changes are present—ECG changes indicate urgent need regardless of the exact potassium value 1
• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
• Do not use sodium bicarbonate in patients without metabolic acidosis—it is only indicated when acidosis is present 1
• Ensure glucose is administered with insulin to prevent hypoglycemia 1
• Remember that calcium, insulin, and beta-agonists do not remove potassium from the body—they only temporize 1
• Never permanently discontinue RAAS inhibitors in CKD patients due to hyperkalemia—use potassium binders to enable continuation of these life-saving medications 1
• Avoid sodium polystyrene sulfonate (Kayexalate) for acute management due to delayed onset, limited efficacy, and risk of bowel necrosis 1

Team Approach

Optimal chronic hyperkalemia management involves a multidisciplinary team including nephrologists, cardiologists, primary care physicians, nurses, pharmacists, and dietitians. 1