What are the initial steps in managing Acute Kidney Injury (AKI)?

Initial Management of Acute Kidney Injury

Immediately discontinue all nephrotoxic medications and diuretics, then identify and treat the underlying cause while optimizing hemodynamics with isotonic crystalloids—this takes priority over all other interventions. 1

Step 1: Immediate Medication Review and Withdrawal

• Stop all nephrotoxic drugs immediately, including NSAIDs, aminoglycosides, ACE inhibitors, ARBs, diuretics, beta-blockers, vasodilators, and iodinated contrast media 1
• Review all medications including over-the-counter drugs that may contribute to kidney injury 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 3

Critical pitfall: Never use furosemide in hemodynamically unstable patients with prerenal AKI—it worsens volume depletion and reduces renal perfusion 1

Step 2: Assess and Optimize Volume Status

• Use isotonic crystalloids (preferably lactated Ringer's over 0.9% saline) as first-line therapy for volume expansion in patients with clinically suspected hypovolemia 1
• Avoid hydroxyethyl starches as they increase the risk of worsening AKI 3, 1
• Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion 3, 1
• Use dynamic indices (passive leg-raising test, pulse/stroke volume variation) rather than static measurements to guide fluid therapy 1
• Monitor for fluid overload using urine output, vital signs, and when indicated, echocardiography or CVP 3

Critical pitfall: Volume overload worsens outcomes in AKI, so attention must be paid to overall fluid balance 4

Step 3: Identify and Treat Precipitating Factors

• Promptly recognize and treat bacterial infections when diagnosed or strongly suspected 2
• Treat gastrointestinal bleeding with blood products if this precipitated the AKI 2
• Rule out urinary tract obstruction through clinical assessment; avoid indwelling bladder catheterization unless necessary 2
• Measure urine volume as oliguria is associated with poor prognosis 2

Step 4: Stage-Specific Management (For Cirrhotic Patients)

For AKI Stage 1A (creatinine <1.5 mg/dL):

• Close monitoring with serum creatinine every 2-4 days during hospitalization 2
• Continue medication withdrawal and volume expansion as above 5

For AKI Stage 1B, 2, or 3 (creatinine ≥1.5 mg/dL):

• Administer IV albumin 1 g/kg bodyweight (maximum 100g) for two consecutive days to differentiate prerenal AKI from hepatorenal syndrome 5, 1
• If no response after 2 days and patient meets HRS criteria, initiate vasoconstrictors (terlipressin, norepinephrine, or midodrine plus octreotide) plus albumin 5, 3
• Earlier initiation of vasoconstrictors in hepatorenal syndrome-AKI leads to better response rates 1

Important nuance: Most experts have concerns about using vasoconstrictors in patients with AKI stage 1 and serum creatinine <1.5 mg/dL 2

Step 5: Hemodynamic Optimization

• Use vasopressors in conjunction with fluids for vasomotor shock 3
• Prefer norepinephrine over dopamine as first-line vasopressor 3
• Do not use dopamine to prevent or treat AKI—it has no benefit based on level 1A/B evidence 1
• Earlier use of vasoactive medications may be appropriate instead of excessive fluid administration for hypotension 1

Step 6: Monitoring and Reassessment

• Monitor 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
• If AKI persists or progresses, reassess the underlying etiology and consider nephrology consultation 3
• Re-evaluate hemodynamic and volume status, adequacy of kidney perfusion, and identify complications such as fluid overload, acidosis, and hyperkalemia 3

Critical pitfall: Do not use eGFR equations designed for CKD to assess renal function in AKI—they are inaccurate in this setting 1

Step 7: Consider Renal Replacement Therapy

• Individualize timing of RRT based on overall clinical condition rather than specific creatinine or BUN thresholds 3, 1
• Consider RRT for refractory hyperkalemia, volume overload, intractable acidosis, uremic complications, or toxin removal 3
• Recent studies suggest no consistent benefit to early-start dialysis 6

What Does NOT Work (High-Quality Evidence)

• Do not use dopamine, diuretics (except for volume overload after adequate perfusion), N-acetylcysteine, or recombinant human insulin-like growth factor 1 for AKI treatment 1
• There are currently no targeted pharmacotherapies approved for the treatment of AKI itself 4

Follow-Up After Initial Management

• Continue nephrotoxin avoidance during the recovery phase to prevent re-injury 3
• Assess serum creatinine every 2-4 days during hospitalization and at least every 2-4 weeks during the first 6 months after discharge 2
• Educate patients to avoid taking NSAIDs or new medications without consulting their healthcare provider 3