Treatment of Prerenal Acute Kidney Injury
The primary treatment for prerenal acute kidney injury (AKI) is to identify and correct the underlying cause of decreased renal perfusion through volume expansion in hypovolemic patients, discontinuation of nephrotoxic medications, and restoration of adequate blood pressure. 1
Initial Management
- Immediately review all medications and withdraw potential nephrotoxic agents including diuretics, NSAIDs, ACE inhibitors, ARBs, and vasodilators 2, 1
- Perform plasma volume expansion in patients with clinically suspected hypovolemia using isotonic crystalloids as first-line fluid therapy 1
- Target a mean arterial pressure of at least 65 mmHg to ensure adequate renal perfusion 1
- For patients with cirrhosis and ascites with prerenal AKI, administer intravenous albumin at 1 g/kg bodyweight (maximum 100 g) for two consecutive days 2
- Identify and treat underlying causes such as infections, gastrointestinal bleeding, or excessive diuresis 2
Fluid Management
- Use isotonic crystalloids rather than colloids as initial management for volume expansion in most cases of prerenal AKI 1
- For patients with acute gastrointestinal bleeding, administer packed red blood cells to maintain hemoglobin levels between 7-9 g/dL 2
- In patients with tense ascites, perform therapeutic paracentesis with albumin infusion to improve renal function 2
- Monitor for signs of fluid overload using urine output, vital signs, and when indicated, echocardiography 1
- Avoid hydroxyethyl starches due to increased risk of worsening AKI 1
Medication Management
- Discontinue the "triple whammy" combination of NSAIDs, diuretics, and ACE inhibitors/ARBs, which significantly increases AKI risk 2, 1
- Do not use diuretics to treat prerenal AKI except for managing volume overload after adequate renal perfusion has been restored 1
- Be cautious with nephrotoxic antibiotics (aminoglycosides, vancomycin), contrast agents, and other potentially nephrotoxic drugs 2
- Remember that each additional nephrotoxin increases the odds of developing AKI by 53%, with risk compounding when multiple nephrotoxins are used 2, 1
Special Considerations for Cirrhotic Patients
- For patients with cirrhosis and prerenal AKI, discontinue beta-blockers in addition to diuretics 2
- In hepatorenal syndrome AKI (HRS-AKI), after ruling out other causes and if not responding to volume expansion, administer vasoconstrictors (terlipressin, norepinephrine, or midodrine plus octreotide) along with albumin 2, 1
- For large volume paracentesis (>5 L), administer IV albumin to prevent post-paracentesis circulatory dysfunction and subsequent AKI 2
- In patients with spontaneous bacterial peritonitis, administer albumin infusion according to current guidelines to prevent AKI 2
Monitoring and Follow-up
- Closely monitor renal function and urine output, particularly in the first 48-72 hours 2, 1
- Measure electrolytes every 12-24 hours during acute management 1
- Reassess the etiology and consider nephrology consultation for patients with persistent AKI (>48 hours) 2, 1
- Continue nephrotoxin avoidance during the recovery phase to prevent re-injury 2, 1
Common Pitfalls to Avoid
- Avoid using furosemide in hemodynamically unstable patients with prerenal AKI, as it can worsen volume depletion and further reduce renal perfusion 1
- Do not delay fluid resuscitation in hypovolemic patients with prerenal AKI 1
- Avoid combining multiple nephrotoxic medications, especially in high-risk patients 2
- Do not use eGFR equations designed for chronic kidney disease to assess renal function in AKI, as they are inaccurate in this setting 1
Management Based on AKI Stage
- For Stage 1 AKI: Remove risk factors, provide volume expansion if hypovolemic, and closely monitor renal function 2
- For Stage 2-3 AKI: Consider vasopressor therapy if fluid resuscitation fails to restore adequate blood pressure 2, 1
- For persistent AKI despite appropriate interventions, consider renal replacement therapy based on the patient's overall clinical condition 1