How to manage acute kidney injury in rheumatic heart disease?

Management of Acute Kidney Injury in Rheumatic Heart Disease

The management of acute kidney injury (AKI) in rheumatic heart disease requires prompt hemodynamic optimization, careful fluid management, and avoidance of nephrotoxic agents to improve outcomes related to morbidity, mortality, and quality of life. 1

Initial Assessment and Classification

• Classify the severity of AKI using standardized staging criteria (increases in serum creatinine of ≥0.3 mg/dL within 48 hours, or ≥1.5 times baseline, or urine output <0.5 mL/kg/h for 6-12 hours) 1
• Determine if AKI is primarily due to cardiorenal syndrome (type 1) which occurs in up to one-third of patients with acute heart failure 1
• Assess for risk factors that predispose to AKI in rheumatic heart disease, including hypotension, use of intra-aortic balloon pump, chronic heart failure, age >75 years, anemia, diabetes, and contrast exposure 1

Hemodynamic Optimization

• Improve cardiac output and renal perfusion through careful management of preload, afterload, and contractility 1
• Consider inotropic support in patients with low cardiac output to improve renal perfusion while maintaining adequate systemic blood pressure 1
• Optimize pulmonary vasodilator therapy for patients with pulmonary hypertension and right ventricular failure, which is common in rheumatic heart disease 1
• Monitor central venous pressure, as excessive venous congestion can worsen renal function through increased renal venous pressure 2

Fluid Management

• Carefully assess volume status, as both hypovolemia and hypervolemia can worsen kidney function in rheumatic heart disease 1
• For volume overload, implement judicious diuresis with loop diuretics, recognizing that transient increases in creatinine during decongestion may be acceptable if associated with clinical improvement 2
• Consider combination diuretic therapy (loop diuretics with thiazides) for diuretic resistance in patients with CKD stages 3 and 4 3
• Monitor for signs of fluid overload using clinical assessment and potentially newer techniques to detect volume status 1

Renal Replacement Therapy Considerations

• Consider renal replacement therapy (RRT) for diuretic-resistant fluid overload, severe metabolic derangements, or progressive uremia 4
• For patients with hemodynamic instability (common in rheumatic heart disease with AKI), continuous renal replacement therapy may be preferred over intermittent hemodialysis 4
• Isolated ultrafiltration with individualized rates may be considered for diuretic-resistant patients but should not be used as initial therapy 5
• For patients requiring both extracorporeal life support and RRT, coordinate anticoagulation strategies carefully 1

Medication Management

• Implement a nephrotoxic medication stewardship program that includes 1:
  • Medication regimen review with evaluation of pharmacokinetic/pharmacodynamic interactions
  • Assessment of the impact of AKI on drug metabolism
  • Dynamic prescription adjustments during transitions of care
• Consider temporary discontinuation of nephrotoxic agents when 1:
  • The agent is determined to be the potential cause of AKI
  • A suitable and less nephrotoxic alternative is available
  • The agent is considered non-essential
• Carefully evaluate the risk-benefit ratio of renin-angiotensin-aldosterone system inhibitors 1:
  • These may need temporary discontinuation during acute decompensation
  • Consider restarting when GFR has stabilized and volume status is optimized
  • Abrupt discontinuation may lead to rebound hypertension and cardiac decompensation

Special Considerations for Rheumatic Heart Disease

• Address valvular dysfunction, which is the hallmark of rheumatic heart disease and can contribute to AKI through hemodynamic derangements 1
• For patients with concomitant acute coronary syndrome, follow acute coronary syndrome guidelines with urgent coronary angiography and revascularization as appropriate, with careful attention to contrast use 1
• Consider tricuspid valve repair/replacement for severe tricuspid regurgitation contributing to volume overload and venous congestion 1
• Evaluate for pulmonary hypertension, which is common in rheumatic heart disease and can lead to right ventricular failure and subsequent kidney dysfunction 1

Long-term Management and Follow-up

• Monitor for progression to chronic kidney disease, as post-AKI proteinuria is associated with future loss of kidney function 1
• Implement shared decision-making and communication among caregivers, the patient, and family members 1
• Consider multidisciplinary care involving both cardiology and nephrology for patients with heart failure and kidney dysfunction 3
• Avoid nephrotoxins and limit contrast exposure during follow-up imaging 1

Pitfalls and Caveats

• Do not automatically discontinue guideline-directed medical therapies for heart failure when mild increases in creatinine occur during decongestion, as this may worsen long-term outcomes 2
• Recognize that not all increases in creatinine represent tubular injury; some reflect hemodynamic changes that may be necessary for effective decongestion 2
• Avoid excessive fluid removal rates that may lead to intravascular volume depletion and worsen kidney function 1
• Be aware that patients with rheumatic heart disease often have multiple comorbidities that can complicate management of AKI 1

By following this structured approach to managing AKI in rheumatic heart disease, clinicians can optimize outcomes while minimizing complications related to both cardiac and renal dysfunction.