What is the treatment approach for post-operative Acute Kidney Injury (AKI)?

Treatment Approach for Post-operative Acute Kidney Injury (AKI)

The treatment of post-operative AKI should focus on identifying and treating the underlying cause, avoiding nephrotoxins, optimizing fluid status with crystalloids, and implementing goal-directed hemodynamic management to reduce morbidity and mortality. 1

Initial Assessment and Management

• Immediately review all medications and withdraw nephrotoxic drugs, diuretics, vasodilators, and NSAIDs that may worsen kidney function 1
• Perform plasma volume expansion in patients with clinically suspected hypovolemia using isotonic crystalloids (not colloids) as first-line fluid therapy 2, 1
• Target mean arterial pressure of at least 65 mmHg to ensure adequate renal perfusion in prerenal AKI 1
• Avoid the "triple whammy" combination of NSAIDs, diuretics, and ACE inhibitors/ARBs, which significantly increases AKI risk 1
• Consider urinary biomarkers (tissue inhibitor of metalloproteinases-2 and insulin-like growth factor-binding protein 7) to identify patients at increased risk of developing AKI as early as 1 hour after cardiopulmonary bypass 2

Fluid Management

• Use isotonic crystalloids rather than colloids for initial volume expansion in patients with or at risk for AKI 2
• Avoid hydroxyethyl starches due to their association with increased AKI incidence 2
• Implement goal-directed fluid therapy using standardized algorithms with quantified goals including blood pressure, cardiac index, systemic venous oxygen saturation, and urine output 2
• Monitor for fluid overload using urine output, vital signs, and when indicated, echocardiography 1

Hemodynamic Support

• Consider vasopressor therapy if fluid resuscitation fails to restore adequate blood pressure in Stage 2-3 AKI 1
• For patients with cirrhosis and ascites with AKI, administer intravenous albumin at 1 g/kg bodyweight for two consecutive days 1
• Use goal-directed fluid therapy with monitoring techniques to guide administration of fluids, vasopressors, and inotropes to avoid hypotension and low cardiac output 2

Medication Management

• Discontinue angiotensin-converting enzyme inhibitors and angiotensin II antagonists for 48 hours in patients with positive urinary biomarkers for AKI 2
• Avoid nephrotoxic agents, hyperglycemia, and radiocontrast agents in patients at risk for AKI 2
• Do not use diuretics to prevent or treat AKI except for managing volume overload 1
• Avoid using dopamine, N-acetylcysteine, and recombinant human insulin-like growth factor 1 for treatment of AKI as they have shown no benefit 2

Renal Replacement Therapy (RRT)

• Individualize the timing of RRT based on the patient's overall clinical condition 1
• Consider RRT for patients with severe AKI, particularly those with life-threatening complications such as severe hyperkalemia, metabolic acidosis, or volume overload unresponsive to diuretics 3

Monitoring and Follow-up

• Monitor electrolytes every 12-24 hours during acute management 1
• Reassess the etiology and consider nephrology consultation for patients with persistent AKI (>48 hours) 1
• Use timed urine creatinine clearance rather than eGFR equations (MDRD, CKD-EPI) for assessment of kidney function in persistent AKI 1
• Implement clinical follow-up after AKI, particularly for patients with severe AKI (requiring temporary RRT) or persisting renal dysfunction at hospital discharge 2

Prevention of AKI Progression

• Continue nephrotoxin avoidance during the recovery phase to prevent re-injury 1
• Closely monitor renal function and urine output, especially in Stage 1 AKI 1
• Recognize that AKI can progress to acute kidney disease (AKD) if recovery is incomplete, requiring continued monitoring beyond the acute phase 4

Special Considerations for Obstructive AKI

• Perform renal ultrasound to identify hydronephrosis and the level of obstruction when obstructive causes are suspected 4
• Treat the underlying cause of obstruction, such as stones, tumor, or stricture 4
• Monitor for post-obstructive diuresis, which may lead to volume depletion and electrolyte abnormalities 4

Common Pitfalls to Avoid

• Do not use furosemide in hemodynamically unstable patients with AKI, as it can precipitate volume depletion and further renal hypoperfusion 1
• Avoid using eGFR equations designed for chronic kidney disease to assess renal function in AKI 1
• Recognize that each additional nephrotoxin increases the odds of developing AKI by 53% 1
• Do not delay treatment of the underlying cause, as AKI is strongly linked to increased risk for chronic kidney disease, subsequent AKI, and future mortality 3