What is the recommended treatment approach for acute kidney injury?

Treatment for Acute Kidney Injury

Immediately discontinue all nephrotoxic medications—including NSAIDs, ACE inhibitors, ARBs, diuretics, beta-blockers, aminoglycosides, and contrast agents—as this is the single most important initial intervention that takes priority over all other treatments. 1, 2

Initial Management: Medication Review and Nephrotoxin Elimination

• Stop nephrotoxic drugs within the first hour of AKI diagnosis, as each additional nephrotoxin increases AKI odds by 53%. 1, 2
• The "triple whammy" combination (NSAIDs + diuretics + ACE inhibitors/ARBs) is particularly dangerous and must be discontinued immediately. 1, 2
• Review all prescription and over-the-counter medications to identify hidden nephrotoxins. 1, 2
• Rule out urinary tract obstruction through clinical assessment or renal ultrasonography before proceeding with other interventions. 2

Common pitfall: Do not use furosemide in hemodynamically unstable patients with prerenal AKI—it worsens volume depletion and reduces renal perfusion. 2

Fluid Management and Hemodynamic Optimization

For Prerenal AKI (Hypovolemia)

• Use isotonic crystalloids as first-line therapy, preferentially choosing balanced solutions (lactated Ringer's) over 0.9% saline to prevent metabolic acidosis and hyperchloremia. 1, 2
• Avoid hydroxyethyl starches entirely, as they are associated with worsening AKI and increased mortality. 1, 2, 3
• 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 like CVP to guide fluid therapy. 2

Expected timeline: Prerenal AKI should show creatinine improvement within 48 hours of adequate volume expansion; lack of improvement suggests acute tubular necrosis or intrinsic kidney disease. 2

Vasopressor Therapy

• If fluid resuscitation fails to restore adequate blood pressure, use norepinephrine as first-line vasopressor (not dopamine). 1, 2
• Consider earlier use of vasoactive medications instead of excessive fluid administration when hypotension persists. 2
• Do NOT use dopamine to prevent or treat AKI—this is ineffective based on Level 1A evidence. 2, 4

Volume Overload Prevention

• Avoid excessive fluid administration that leads to volume overload >10-15% body weight, as this is associated with adverse outcomes. 2
• Monitor for fluid overload using urine output, vital signs, and when indicated, echocardiography or CVP. 1

Special Population: Cirrhotic Patients with AKI

Initial Management (All Stages)

• Discontinue BOTH diuretics AND beta-blockers immediately (unlike other populations where only diuretics are stopped). 1, 2
• Administer IV albumin 1 g/kg bodyweight (maximum 100g) daily for two consecutive days. 1, 2, 5

Stage-Based Approach

Stage 1A AKI (creatinine rise >0.3 mg/dL but <2× baseline):

• Remove precipitating factors, provide volume expansion if hypovolemic, and monitor serum creatinine every 2-4 days. 2
• Vasoconstrictors are NOT indicated unless creatinine reaches ≥1.5 mg/dL. 2

Stage 2-3 AKI (creatinine ≥2× baseline or ≥1.5 mg/dL):

• After albumin administration for 2 days, if creatinine remains elevated and hepatorenal syndrome criteria are met, add vasoconstrictor therapy (terlipressin, norepinephrine, or midodrine plus octreotide) together with continued albumin. 1, 2, 5
• Earlier initiation of vasoconstrictors improves response rates, as higher baseline creatinine predicts lower treatment success. 2

Additional Cirrhosis-Specific Interventions

• Therapeutic paracentesis combined with albumin infusion improves renal function in patients with tense ascites. 2
• Albumin infusion during spontaneous bacterial peritonitis prevents development of AKI. 2

Monitoring and Reassessment for Persistent AKI

• Reassess the underlying etiology of AKI if it persists beyond 48 hours from onset. 6, 1
• Re-evaluate hemodynamic and volume status, adequacy of kidney perfusion, and identify complications such as fluid overload, acidosis, and hyperkalemia. 6, 1
• Measure serum creatinine and electrolytes every 12-24 hours during acute management. 2
• Consider nephrology consultation if the etiology is unclear or subspecialist care is needed. 6, 1

Important caveat: 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. 2

Ineffective Therapies to Avoid

Based on Level 1A/B evidence, do NOT use the following interventions:

• Dopamine for AKI prevention or treatment 1, 2
• N-acetylcysteine (NAC) 2
• Loop diuretics to treat AKI (except for managing volume overload after adequate renal perfusion is restored) 2
• Recombinant human insulin-like growth factor 1 2

Indications for Renal Replacement Therapy

Initiate RRT when any of the following absolute indications occur despite optimal medical management:

• Refractory hyperkalemia unresponsive to medical therapy 1, 5

• Severe volume overload causing pulmonary edema or respiratory compromise 1, 5

• Intractable metabolic acidosis (e.g., pH <7.1) 1, 5

• Uremic complications (encephalopathy, pericarditis, bleeding) 1, 5

• Do not delay RRT when absolute indications are present, as postponement is associated with increased mortality. 1

• Timing of RRT should be based on overall clinical condition rather than specific creatinine or BUN thresholds alone. 1, 2

• Reassess the need for ongoing RRT daily rather than adhering to a fixed schedule. 1

Management of Specific Complications

• Manage hyperkalemia with insulin/glucose, calcium gluconate, sodium bicarbonate, potassium binders, or RRT in severe cases. 5
• Treat bacterial infections promptly when diagnosed or strongly suspected. 2
• Manage gastrointestinal bleeding with blood products if it precipitated the AKI. 2

Follow-Up and Recovery Phase

• Continue nephrotoxin avoidance during the recovery phase of acute kidney disease (AKD) to prevent re-injury. 1
• Monitor for development or progression of chronic kidney disease, as even patients with complete recovery remain at increased risk. 2, 5
• For cirrhotic patients with Stage 1A AKI, check serum creatinine every 2-4 days during hospitalization and every 2-4 weeks for six months after discharge. 2
• Educate patients to avoid NSAIDs or new medications without consulting their healthcare provider. 1

Key Differentiating Strategy: Prerenal AKI vs. Acute Tubular Necrosis

• Discontinue diuretics and nephrotoxic drugs, provide volume expansion (crystalloids or albumin in cirrhosis), then re-evaluate renal function at 48 hours. 2
• A creatinine decline indicates prerenal AKI; absence of change points to acute tubular necrosis or intrinsic disease. 2
• Urinary neutrophil gelatinase-associated lipocalin (NGAL) reliably distinguishes ATN from prerenal causes, including hepatorenal syndrome. 2