What is the treatment for acute kidney injury (AKI)?

Treatment of Acute Kidney Injury

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

Immediate Medication Management

Stop all nephrotoxic drugs immediately, including: 1

• NSAIDs
• Aminoglycosides
• ACE inhibitors/ARBs
• Diuretics
• Beta-blockers
• Vasodilators
• Iodinated contrast media

The "triple whammy" combination (NSAIDs + diuretics + ACE inhibitors/ARBs) is particularly dangerous and must be discontinued immediately. 1 Each additional nephrotoxic agent increases AKI odds by 53%, so avoid combining multiple nephrotoxic drugs. 1

Critical Pitfall to Avoid

Never use furosemide in hemodynamically unstable patients with prerenal AKI—it worsens volume depletion and reduces renal perfusion. 1 Diuretics should only be used for managing volume overload after adequate renal perfusion is restored. 1

Fluid Resuscitation and Hemodynamic Management

Use isotonic crystalloids (preferably lactated Ringer's over 0.9% saline) as first-line therapy for volume expansion in prerenal AKI. 2, 1 Avoid 0.9% saline when possible to prevent metabolic acidosis and hyperchloremia. 3

Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion. 1 However, fluid administration must be judicious—indiscriminate fluid administration may worsen outcomes and delay recovery. 3

Fluid Assessment Strategy

• Use dynamic indices (passive leg-raising test, pulse/stroke volume variation) rather than static measurements to guide fluid therapy 1
• Monitor fluid status through clinical examination and daily fluid balance with accurate intake/output documentation 3
• Use echocardiography or CVP when indicated to assess volume status and prevent fluid overload 1
• Consider earlier use of vasoactive medications instead of excessive fluid administration for hypotension 1

What NOT to Use

Avoid hydroxyethyl starches—they increase the risk of worsening AKI. 1 While some specific subgroups may receive albumin (severe hypoalbuminemia, cirrhosis with spontaneous bacterial peritonitis), isotonic crystalloids remain first-line for most patients. 2

Potential Harm from Excessive Fluids

Early large-volume crystalloid administration predicts secondary abdominal compartment syndrome, and aggressive resuscitation may be detrimental for patients with ischemic or mixed etiology ATN. 3 The incidence of coagulopathy increases with increasing IV fluid volume. 3

Special Population: Cirrhotic Patients

In cirrhotic patients with AKI, discontinue BOTH diuretics AND beta-blockers (not just diuretics). 1 This is a critical distinction from general AKI management.

Administer IV albumin 1 g/kg bodyweight (maximum 100g) for two consecutive days to differentiate prerenal AKI from hepatorenal syndrome. 2, 1 The maximal dose per day should not exceed 100g. 2

For hepatorenal syndrome-AKI specifically, treatment should not be delayed until creatinine reaches 2.5 mg/dL—initiate vasoconstrictors (terlipressin or norepinephrine or midodrine plus octreotide) and albumin earlier, as higher creatinine at treatment initiation leads to lower response rates. 2

Monitoring Requirements

Measure serum creatinine and electrolytes (sodium, potassium, bicarbonate) every 12-24 hours during acute management. 1 For deteriorating patients, check at least every 48 hours or more frequently. 3

Monitor closely in the first 48-72 hours: 1

• Urine output
• Vital signs
• Fluid balance
• Signs of volume depletion (tachycardia, hypotension, decreased urine output, worsening renal function) 3

Critical Assessment Error to Avoid

Do not use eGFR equations designed for CKD to assess renal function in AKI—they are inaccurate in this setting. 1 Physical examination alone has limitations for differentiating between prerenal and parenchymal AKI. 3

Renal Replacement Therapy Considerations

Individualize timing of RRT based on overall clinical condition rather than specific creatinine or BUN thresholds. 1 Consider RRT for persistent AKI despite appropriate interventions, based on the patient's clinical status. 1 Studies have not consistently demonstrated benefit to early-start dialysis. 4

What Does NOT Work (High-Quality Evidence)

Based on level 1A/B evidence, do NOT use the following agents for AKI treatment: 2

• Dopamine
• Diuretics (for treatment of AKI itself)
• N-acetylcysteine (NAC)
• Recombinant human insulin-like growth factor 1 (IGF-1)

These recommendations are based on negative efficacy trials and represent areas where practice should definitively change. 2

Polyuric Phase Management

During the polyuric phase of ATN, replace ongoing fluid losses with appropriate crystalloid solutions to maintain euvolemia. 3 Calculate ongoing losses (urine output + insensible losses + other losses) and replace 80-100% of measured losses. 3

Key Conceptual Error to Avoid

Do not misinterpret "pre-renal" as simply "hypovolemic"—this leads to indiscriminate fluid administration when the actual problem may be more complex. 3 Ensuring adequate hydration is essential, but volume status must be repeatedly reassessed based on hemodynamic parameters rather than fixed regimens. 3