Management of Worsening Kidney Function in Dialysis Patients with Heart Failure
For patients already on dialysis with heart failure experiencing worsening kidney function, focus on optimizing volume status through dialysis prescription adjustments, continuing guideline-directed medical therapy (GDMT) with careful monitoring, and addressing reversible causes of hemodynamic instability rather than withdrawing life-saving medications. 1
Immediate Assessment Priorities
Volume Status Evaluation
- Assess for persistent congestion using clinical examination (jugular venous distension, peripheral edema, pulmonary crackles) and point-of-care ultrasound including inferior vena cava assessment and Venous Excess Ultrasound (VEXUS) score. 1
- Congestion remains the primary driver of worsening outcomes in dialysis patients with heart failure, and inadequate decongestion increases mortality risk. 1
- Distinguish between true volume overload versus low cardiac output states, as management differs fundamentally—if uncertainty exists, right heart catheterization should be performed to guide therapy. 1
Hemodynamic Assessment
- Check blood pressure and assess for signs of low cardiac output (altered mentation, cool extremities, oliguria despite adequate dialysis). 1
- In dialysis patients with heart failure, both volume overload and inadequate perfusion can present with rising creatinine, making clinical assessment critical. 1
Dialysis Prescription Optimization
Ultrafiltration Strategy
- Adjust ultrafiltration rate to achieve euvolemia gradually—avoid ultrafiltration rates exceeding 13 mL/kg/hour as higher rates associate with intradialytic hypotension, organ ischemia, and cardiovascular events. 1, 2
- Consider extending dialysis session duration or increasing frequency (e.g., adding temporary extra sessions) rather than aggressive ultrafiltration during single sessions to safely remove excess volume. 2
- The CARRESS-HF trial demonstrated that adjustable ultrafiltration with high rates led to worsening kidney function and adverse events, emphasizing the importance of gradual volume removal. 1
Dialysate Modifications
- Use cooler dialysate temperature (35-36°C) to improve hemodynamic stability and reduce intradialytic hypotension risk. 3
- Adjust dialysate sodium and potassium concentrations to minimize electrolyte fluctuations that trigger arrhythmias, particularly in the 4-5 hours post-dialysis when dysrhythmogenic risk peaks. 3
Modality Considerations
- Hemodialysis demonstrates superior survival compared to peritoneal dialysis in patients with end-stage renal disease and congestive heart failure (median survival 36.7 vs 20.4 months, adjusted HR 1.48). 4
- While peritoneal dialysis offers gentler fluid removal, the survival disadvantage in heart failure patients makes hemodialysis the preferred modality. 4, 5
Guideline-Directed Medical Therapy Management
Continue Life-Saving Medications
- Do NOT discontinue ACE inhibitors, ARBs, or mineralocorticoid receptor antagonists (MRAs) solely due to rising creatinine in dialysis patients—these medications provide mortality benefit in heart failure regardless of kidney function. 1, 6
- In dialysis patients, traditional concerns about hyperkalemia and worsening kidney function become less relevant as dialysis manages both. 1
Medication Adjustments
- For ACE inhibitors/ARBs: Continue at current doses in dialysis patients with heart failure, as renal function no longer dictates dosing. 7
- For MRAs: Monitor potassium closely but continue therapy—if potassium exceeds 6.0 mmol/L, temporarily hold MRA and adjust dialysate potassium rather than permanently discontinuing. 1
- Beta-blockers should be continued and optimized after volume status stabilizes, as they reduce sudden cardiac death risk in dialysis patients. 1, 3
Hyperkalemia Management in Dialysis Patients
- If hyperkalemia develops (K+ >5.5 mmol/L), adjust dialysate potassium concentration to 2-3 mEq/L rather than discontinuing GDMT. 1
- Consider newer potassium binders (patiromer or sodium zirconium cyclosilicate) to maintain RAAS inhibitor therapy if hyperkalemia persists despite dialysate adjustments. 1, 8
- Avoid sodium polystyrene sulfonate (Kayexalate) due to serious gastrointestinal adverse events, particularly in elderly dialysis patients. 8
Addressing Reversible Causes
Medication Review
- Discontinue nephrotoxic agents: NSAIDs, aminoglycosides, contrast agents, and other nephrotoxins that may precipitate acute-on-chronic kidney injury. 1
- NSAIDs cause sodium retention, worsen heart failure, and should be avoided entirely in this population. 1
Cardiac Optimization
- Evaluate for active ischemia, arrhythmias (particularly atrial fibrillation), or valvular disease that may be precipitating heart failure decompensation. 1
- Perform baseline ECG and consider echocardiography to assess left ventricular function and identify structural abnormalities. 1
- Dialysis patients have 80% prevalence of left ventricular hypertrophy, which impairs diastolic filling and increases arrhythmia risk. 1, 3
Infection and Metabolic Screening
- Rule out intercurrent illness (infection, anemia exacerbation, thyroid dysfunction) that may trigger heart failure decompensation. 1
- Dialysis patients experience dynamic electrolyte shifts that can precipitate dysrhythmias and hemodynamic instability. 3
Monitoring Strategy
Frequency of Assessment
- Monitor volume status clinically at each dialysis session, adjusting ultrafiltration goals based on symptoms, weight trends, and blood pressure response. 1, 2
- Check electrolytes (particularly potassium and magnesium) weekly during acute decompensation, then monthly once stable. 1, 3
- Assess for intradialytic hypotension and post-dialysis symptoms, as these indicate excessive ultrafiltration or inadequate cardiac output. 1, 2
Biomarker Utilization
- Consider BNP/NT-proBNP trends to assess adequacy of decongestion, though absolute values are less reliable in dialysis patients. 1
- Rising biomarkers despite dialysis suggest persistent congestion requiring more aggressive volume management. 1
Critical Pitfalls to Avoid
Do Not Withdraw GDMT Prematurely
- The most common error is discontinuing ACE inhibitors, ARBs, or MRAs due to rising creatinine in dialysis patients—these medications improve survival regardless of kidney function. 1, 6
- In dialysis patients, creatinine changes reflect residual renal function loss, not medication toxicity. 1
Avoid Aggressive Ultrafiltration
- Rapid ultrafiltration (>13 mL/kg/hour) causes intradialytic hypotension, myocardial stunning, gut ischemia, and paradoxically worsens outcomes. 1, 2
- The AVOID trial showed adjustable ultrafiltration with gradual volume removal prevents complications. 1
Do Not Ignore Low Cardiac Output
- If worsening kidney function occurs with hypotension, cool extremities, or altered mentation, suspect low cardiac output rather than volume overload—these patients may require inotropic support or mechanical circulatory support, not more ultrafiltration. 1
- Right heart catheterization clarifies hemodynamics when clinical assessment is uncertain. 1
Avoid Triple RAAS Blockade
- Never combine ACE inhibitor + ARB + MRA, as this dramatically increases hyperkalemia risk without additional benefit. 1
- Dual therapy (ACE inhibitor or ARB + MRA) provides optimal outcomes in heart failure. 1
Special Considerations for Dialysis Patients
Residual Renal Function Preservation
- Avoid excessive ultrafiltration and hypotensive episodes, as these accelerate loss of residual renal function, which associates with better survival in dialysis patients. 2
- Gradual volume reduction with extended or more frequent sessions preserves residual function. 2
Cardiovascular Risk Mitigation
- Target strict volume control to achieve regression of left ventricular hypertrophy and prevent heart failure progression, but do so gradually over weeks to months. 2
- Restriction of dietary sodium intake (<2 grams daily) facilitates volume control with lower ultrafiltration requirements. 2