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

Treatment of Acute Kidney Injury

Immediate Priority: Stop All Nephrotoxic Medications

The first and most critical intervention is to immediately discontinue all nephrotoxic medications—this takes absolute priority over all other treatments. 1

Medications to Stop Immediately:

• NSAIDs, aminoglycosides, ACE inhibitors, ARBs, diuretics, beta-blockers, vasodilators, and iodinated contrast media must be discontinued without delay 1
• The "triple whammy" combination (NSAIDs + diuretics + ACE inhibitors/ARBs) is particularly dangerous and represents a medical emergency requiring immediate cessation 1
• Each additional nephrotoxic agent increases AKI odds by 53%, so avoid combining multiple nephrotoxic drugs 1
• Review ALL medications including over-the-counter drugs that may contribute to kidney injury 1, 2

Fluid Management Strategy

First-Line Fluid Therapy:

Use isotonic crystalloids (preferably lactated Ringer's over 0.9% saline) as first-line therapy for volume expansion in hypovolemic patients. 1, 3

• Balanced crystalloids are preferred over 0.9% saline to prevent metabolic acidosis and hyperchloremia 1
• Avoid hydroxyethyl starches completely—they increase the risk of worsening AKI and mortality 1, 4
• Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion 1, 3

Dynamic Assessment Approach:

• Base fluid administration on repeated assessment of hemodynamic status using dynamic indices (passive leg-raising test, pulse/stroke volume variation) rather than static measurements 5, 1
• Both the physiological response to fluids and the underlying AKI condition are dynamic over time, requiring continuous reassessment 5, 2
• Avoid indiscriminate fluid administration based solely on the outdated "prerenal" label without proper hemodynamic assessment 5, 2

Critical Caveat on Fluid Overload:

Volume overload >10-15% body weight is associated with adverse outcomes and worsens kidney function. 5, 1

• Monitor for fluid overload using urine output, vital signs, and when indicated, echocardiography or CVP 1, 3
• Earlier use of vasoactive medications may be more appropriate than excessive fluid administration for hypotension 5, 1

Vasopressor Therapy

If fluid resuscitation fails to restore adequate blood pressure, use norepinephrine as first-line vasopressor. 1, 2

• Target MAP ≥65 mmHg 1, 3
• Do NOT use dopamine—it is ineffective for preventing or treating AKI based on level 1A/B evidence 1, 2

Special Population: Cirrhotic Patients

Unique Management Requirements:

In cirrhotic patients with AKI, discontinue BOTH 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 hepatorenal syndrome 1, 3, 2
• For hepatorenal syndrome-AKI not responding to volume expansion, administer vasoconstrictors (terlipressin, norepinephrine, or midodrine plus octreotide) along with albumin 3, 2

Monitoring Protocol

Acute Phase (First 48-72 Hours):

• Measure serum creatinine and electrolytes every 12-24 hours 1, 3
• Monitor urine output, vital signs, and fluid balance closely 1, 3
• Use echocardiography or CVP when indicated to assess volume status 1

What Does NOT Work (High-Quality Evidence)

The following interventions have been proven ineffective and should NOT be used: 1

• Dopamine (level 1A/B evidence)
• Diuretics for treating AKI (except for managing volume overload AFTER adequate renal perfusion is restored)
• N-acetylcysteine (NAC)
• Recombinant human insulin-like growth factor 1

Critical Pitfall to Avoid:

Never use furosemide in hemodynamically unstable patients with prerenal AKI—it worsens volume depletion and reduces renal perfusion. 1, 3

Renal Replacement Therapy Considerations

Consider RRT for persistent AKI despite appropriate interventions, based on the patient's overall clinical status rather than specific creatinine or BUN thresholds. 1, 2

• Indications include refractory hyperkalemia, volume overload, intractable acidosis, or uremic complications 2, 6
• Timing should be individualized based on overall clinical condition 1, 2

Common Diagnostic Pitfall

Do not use eGFR equations (MDRD, CKD-EPI) designed for chronic kidney disease to assess renal function in AKI—they require steady-state creatinine and are inaccurate in acute settings. 1, 3

Conceptual Framework for Classification

The outdated "prerenal/intrinsic/postrenal" terminology is being replaced with a more useful framework that distinguishes between: 5

• Conditions that reduce glomerular function
• Conditions that cause tubular/glomerular injury
• Conditions that do both

This framework helps avoid the misinterpretation of "prerenal" as automatically meaning "hypovolemic," which can lead to inappropriate fluid overload 5