What is the treatment for Acute Kidney Injury (AKI)?

Treatment of Acute Kidney Injury

Immediate First Steps

The cornerstone of AKI treatment is identifying and reversing the underlying cause while immediately discontinuing all nephrotoxic medications—this takes priority over all other interventions. 1, 2

Medication Review and Withdrawal

• Stop all nephrotoxic drugs immediately, including NSAIDs, aminoglycosides, ACE inhibitors, ARBs, diuretics, beta-blockers, vasodilators, and iodinated contrast media 3, 1, 2
• The "triple whammy" combination (NSAIDs + diuretics + ACE inhibitors/ARBs) is particularly dangerous and must be discontinued 1
• Each additional nephrotoxin increases AKI odds by 53%, so avoid combining multiple nephrotoxic agents 1, 2
• Continue nephrotoxin avoidance throughout the recovery phase to prevent re-injury 1, 2

Fluid Management Strategy

For Hypovolemic Patients

• Use isotonic crystalloids as first-line therapy for volume expansion in most cases of prerenal AKI 1, 2
• Avoid hydroxyethyl starches due to increased risk of worsening AKI 1
• Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion 1, 2
• Use dynamic indices (passive leg-raising test, pulse/stroke volume variation) rather than static measurements to guide fluid therapy 3

Critical Caveat on Fluid Administration

The traditional "pre-renal" terminology is misleading and often leads to indiscriminate fluid administration—fluid therapy must be guided by repeated hemodynamic assessment, not reflexive volume loading 3. Both excessive fluid administration and volume overload worsen AKI outcomes 3, 2.

Management Algorithm by AKI Stage

Stage 1 AKI

• Remove all risk factors (nephrotoxic drugs, vasodilators, NSAIDs) 3, 1
• Withdraw or reduce diuretics 3, 1
• Provide plasma volume expansion only if clinically hypovolemic 3, 1
• Monitor closely for progression 3, 1

Stage 2-3 AKI

• Implement all Stage 1 measures if not already done 3
• Administer IV albumin 1 g/kg/day (maximum 100g/day) for two consecutive days 3, 1, 2
• Consider vasopressor therapy if fluid resuscitation fails to restore adequate blood pressure 1, 2
• Reassess etiology and consider nephrology consultation 2

Special Population: Cirrhotic Patients with AKI

Initial Management

• Discontinue diuretics AND beta-blockers (not just diuretics) 1, 2
• Administer IV albumin 1 g/kg bodyweight (maximum 100g) for two consecutive days to differentiate prerenal AKI from other causes 3, 1
• For large volume paracentesis (>5L), give IV albumin to prevent post-paracentesis circulatory dysfunction 1

Hepatorenal Syndrome-AKI (HRS-AKI)

If AKI persists after 2 days of diuretic withdrawal and albumin administration, and other causes are excluded:

• Administer vasoconstrictors (terlipressin, norepinephrine, or midodrine plus octreotide) along with albumin 1, 2
• Ensure absence of shock, proteinuria >500mg/day, microhematuria >50 RBCs/HPF, and normal renal ultrasound before diagnosing HRS-AKI 3

Monitoring Requirements

• Measure serum creatinine and electrolytes every 12-24 hours during acute management 1
• Monitor urine output, vital signs, and fluid balance closely in the first 48-72 hours 1
• Use echocardiography or CVP when indicated to assess volume status and prevent fluid overload 1, 2
• Reassess hemodynamic status repeatedly, as both the physiological response and underlying condition are dynamic 3

Vasopressor Considerations

• Earlier use of vasoactive medications may be appropriate instead of excessive fluid administration for hypotension 3
• The effect of vasopressor strategies on kidney function is context-specific and not clearly defined 3
• Some vasopressors may be more kidney-protective than others, though evidence is still emerging 4

Renal Replacement Therapy

• Individualize timing of RRT based on overall clinical condition rather than specific creatinine or BUN thresholds 2
• Consider RRT for persistent AKI despite appropriate interventions, based on the patient's clinical status 1
• Early initiation of dialysis has not consistently demonstrated benefit in studies 4

Common Pitfalls to Avoid

• Never use furosemide in hemodynamically unstable patients with prerenal AKI—it worsens volume depletion and reduces renal perfusion 1
• Do not delay fluid resuscitation in truly hypovolemic patients 1
• Avoid using eGFR equations designed for CKD to assess renal function in AKI—they are inaccurate in this setting 1
• Do not use diuretics to treat AKI except for managing volume overload after adequate renal perfusion is restored 1

Emerging Diagnostic Tools

The furosemide stress test (FST) may be useful for identifying patients likely to have progressive AKI requiring dialysis, though it requires careful standardization and quality control 3. Urine biomarkers are becoming important for differentiating HRS-AKI from acute tubular necrosis 3.

Long-Term Considerations

• Even one episode of AKI increases risk of cardiovascular disease, chronic kidney disease, and death 5
• Educate patients to avoid NSAIDs or new medications without consulting their healthcare provider 2
• AKI is not self-limited but strongly linked to increased risk for CKD, subsequent AKI episodes, and future mortality 6