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

Treatment of Acute Kidney Injury

The cornerstone of AKI treatment is immediate identification and reversal of the underlying cause while simultaneously discontinuing all nephrotoxic medications—this takes absolute priority over all other interventions. 1, 2

Immediate Medication Management (First Priority)

Stop all nephrotoxic drugs immediately upon AKI diagnosis:

• Discontinue NSAIDs, aminoglycosides, ACE inhibitors, ARBs, diuretics, beta-blockers, and iodinated contrast media 1, 2
• Evaluate nephrotoxins as the potential cause by assessing temporal sequence between drug administration and AKI onset, other possible causes, and response to drug removal 1
• Critical warning: The "triple whammy" combination (NSAIDs + diuretics + ACE inhibitors/ARBs) is particularly dangerous and must be discontinued immediately 1, 2
• Each additional nephrotoxin increases AKI odds by 53%, and combining 3+ nephrotoxins causes AKI in 25% of non-critically ill patients 1, 2

Special consideration for cirrhotic patients: Discontinue BOTH diuretics AND beta-blockers (not just diuretics alone) 1, 2

Fluid Management and Hemodynamic Optimization

Use isotonic crystalloids as first-line therapy for volume expansion in prerenal AKI:

• Lactated Ringer's is preferred over 0.9% saline to prevent metabolic acidosis and hyperchloremia 2
• Never use hydroxyethyl starches—they worsen AKI and are associated with harm 3, 2, 4
• Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion; patients with preexisting hypertension may require higher targets 3, 2, 5
• Use vasopressors (norepinephrine preferred over dopamine) in conjunction with fluids for vasomotor shock if fluid resuscitation fails to restore adequate blood pressure 1, 3

Conservative fluid strategy after initial resuscitation:

• Switch to neutral or negative fluid balance once hemodynamic stabilization is achieved 6, 4
• Volume overload worsens outcomes in AKI—monitor closely using urine output, vital signs, and when indicated, echocardiography or CVP 3, 2
• Interstitial edema delays renal recovery, so avoid overzealous fluid therapy 6

Management of Specific AKI Types

For cirrhotic patients with AKI:

• Administer IV albumin 1 g/kg bodyweight (maximum 100g/day) for two consecutive days to differentiate prerenal AKI from hepatorenal syndrome 1, 3, 2
• If serum creatinine remains elevated despite initial management (suggesting HRS-AKI), add vasoactive agents: terlipressin (1 mg every 4-6 hours, increase to 2 mg if no 25% creatinine reduction by day 3), norepinephrine (0.5 mg/h continuous infusion, titrate up to 3 mg/h), or midodrine (7.5-12.5 mg TID) plus octreotide (100-200 mcg subcutaneously TID) 1, 3
• Continue therapy until serum creatinine returns to within 0.3 mg/dL of baseline for 2 consecutive days or for maximum 14 days 1

What Does NOT Work (Avoid These Interventions)

Do not use the following—they are ineffective or harmful:

• Low-dose dopamine for prevention or treatment of AKI 1, 3, 2
• Furosemide or other diuretics to prevent or treat AKI (exception: use diuretics ONLY for managing volume overload after adequate renal perfusion is restored) 1, 3, 2
• Fenoldopam, atrial natriuretic peptide, or recombinant human IGF-1 1, 2
• N-acetylcysteine for AKI treatment 2

Critical pitfall: Never use furosemide in hemodynamically unstable patients with prerenal AKI—it worsens volume depletion and reduces renal perfusion 2

Monitoring During Acute Management

Measure serum creatinine and electrolytes every 12-24 hours during acute management 2

• Monitor urine output, vital signs, and fluid balance closely in the first 48-72 hours 2
• Stage AKI using established criteria, but base management on overall clinical status, specific cause, trends in kidney function, comorbidities, volume status, and electrolyte disturbances—not stage alone 3
• Use dynamic indices (passive leg-raising test, pulse/stroke volume variation) rather than static measurements to guide fluid therapy 2

Renal Replacement Therapy Indications

Individualize timing of RRT based on overall clinical condition rather than specific creatinine or BUN thresholds 3, 2

• Consider RRT for refractory hyperkalemia, volume overload unresponsive to diuretics, intractable metabolic acidosis, uremic complications (pericarditis, encephalopathy), or toxin removal 3
• In cirrhotic patients, use RRT for: (A) AKI secondary to acute tubular necrosis, (B) HRS-AKI in liver transplant candidates only, or (C) AKI of uncertain etiology on individual basis 1
• Recent studies do not consistently demonstrate benefit to early-start dialysis over waiting for clear indications 7

Recovery Phase Management

Continue nephrotoxin avoidance during the recovery phase to prevent re-injury 1, 3

• Educate patients to avoid NSAIDs or new medications without consulting their healthcare provider 1, 3
• Exercise caution when reintroducing ACE inhibitors/ARBs—the risk-benefit ratio during AKD differs from routine clinical practice 1
• Avoid NSAIDs in elderly patients with creatinine clearance <30 mL/min 1

Common Pitfalls to Avoid

• Do not use eGFR equations designed for CKD to assess renal function in AKI—they are inaccurate in this acute setting 2
• Do not delay fluid resuscitation in truly hypovolemic patients 2
• Do not withhold indicated contrast material solely due to AKI risk—contrast is less commonly the direct cause of AKI than previously thought 5
• Avoid combining multiple nephrotoxic agents, as risk compounds exponentially 1, 2