How to manage persistent hyperkalemia despite Continuous Renal Replacement Therapy (CRRT)?

Managing Persistent Hyperkalemia Despite CRRT

When hyperkalemia persists despite CRRT, immediately optimize the dialysate potassium concentration to zero or minimal levels, increase CRRT intensity, and consider adding intermittent hemodialysis (IHD) for superior potassium clearance, while simultaneously addressing all non-renal sources of potassium including dietary intake, medications, tissue breakdown, and nutritional formulas. 1

Immediate CRRT Optimization

Adjust Dialysate/Replacement Fluid Composition

• Use dialysis solutions with zero or minimal potassium concentration rather than the standard 4 mEq/L potassium-containing solutions typically used to prevent hypokalemia 2
• Standard CRRT solutions contain potassium (4 mEq/L) to prevent treatment-related hypokalemia, but this is counterproductive when treating persistent hyperkalemia 2
• Commercial KRT solutions are available with variable potassium concentrations that can be adjusted based on patient needs 2

Increase CRRT Intensity

• Maximize effluent flow rates to enhance convective and diffusive potassium clearance 2
• Consider increasing blood flow rates if hemodynamically tolerated 1
• Ensure adequate CRRT circuit function without clotting or reduced efficiency 1

Add Intermittent Hemodialysis

If CRRT alone proves insufficient, add intermittent hemodialysis sessions for superior potassium removal. 1

• IHD provides more rapid and reliable potassium clearance than CRRT, removing potassium at rates of 25-50 mEq/hour 3, 4
• A case report demonstrated successful hyperkalemia control only after adding IHD to ongoing CRRT in a patient with massive rhabdomyolysis 1
• Use separate vascular access for IHD when possible to optimize efficacy and avoid interference with CRRT 1
• IHD remains the most reliable method to remove potassium from the body in refractory cases 3, 4

Address Non-Renal Potassium Sources

Modify Nutritional Support

• Switch to "renal" enteral or parenteral formulas with lower potassium content in patients with persistent hyperkalemia 2
• These concentrated formulas contain reduced amounts of potassium, sodium, and phosphorus, making them advantageous for electrolyte disturbances 2
• Review all nutritional intake including total parenteral nutrition, enteral feeds, and any oral intake for potassium content 2

Eliminate Exogenous Potassium

• Discontinue all potassium supplementation (oral, IV, or in fluids) 2
• Review and eliminate potassium-containing medications including potassium-sparing diuretics, ACE inhibitors, ARBs, MRAs, NSAIDs, and trimethoprim-sulfamethoxazole 2
• Avoid salt substitutes and potassium-rich foods if any oral intake is occurring 2

Control Endogenous Potassium Release

• Identify and treat tissue breakdown sources: rhabdomyolysis, tumor lysis syndrome, hemolysis, or massive tissue injury 1, 3
• Optimize metabolic acidosis correction, as acidosis promotes potassium shift from intracellular to extracellular space 2
• Manage hyperglycemia to prevent osmotic potassium shifts 3

Pharmacologic Adjuncts

Potassium Binders

Consider newer potassium binders (sodium zirconium cyclosilicate or patiromer) as adjunctive therapy even in dialysis-dependent patients. 2

• Sodium zirconium cyclosilicate (SZC) demonstrated efficacy in maintaining normal predialysis potassium levels in ESRD patients with persistent hyperkalemia over 8 weeks 2
• SZC reduces serum potassium within 1-2 hours, with significant reductions observed even in severe hyperkalemia (≥6.0 mEq/L) 2
• Patiromer and SZC bind potassium in the GI tract and eliminate it in feces, providing an additional route of potassium removal beyond renal replacement 2
• These agents work independently of kidney function and can complement dialytic therapy 2

Acute Temporizing Measures

While optimizing CRRT and planning IHD, use standard acute hyperkalemia treatments 2, 3:

• Calcium gluconate IV to stabilize cardiac membranes (acts within 1-3 minutes) 2
• Insulin with glucose IV to shift potassium intracellularly (acts within 30 minutes) 2, 3
• Inhaled beta-2 agonists (albuterol) to augment intracellular potassium shift 2, 4
• Sodium bicarbonate only if concurrent metabolic acidosis is present 2

Common Pitfalls to Avoid

• Do not rely on bicarbonate alone for potassium lowering—recent evidence shows it is not efficacious without concurrent metabolic acidosis 4
• Do not use standard potassium-containing (4 mEq/L) CRRT solutions when treating hyperkalemia, as this will limit potassium removal 2
• Do not assume CRRT is always sufficient—some patients with massive potassium loads (rhabdomyolysis, tumor lysis) require the superior clearance of IHD 1
• Verify true hyperkalemia by ruling out pseudohyperkalemia from hemolysis during blood sampling, especially if clinical picture doesn't match 2
• Monitor for rebound hyperkalemia 2-4 hours after temporizing measures (insulin, albuterol), as these only redistribute potassium without removing it from the body 2

Monitoring Strategy

• Check potassium levels every 2-4 hours initially until stable downward trend established 2
• Continuous ECG monitoring for patients with potassium >6.0 mEq/L or any ECG changes 2, 3
• Reassess CRRT circuit patency and efficiency regularly 1
• Monitor for treatment-related complications including hypoglycemia (from insulin), hypokalemia (from aggressive treatment), and edema (from SZC) 2