Treatment for Acute Kidney Injury
The primary treatment for AKI is supportive care focused on identifying and treating the underlying cause, optimizing fluid and hemodynamic status, discontinuing nephrotoxic medications, and initiating renal replacement therapy when specific indications are met. 1
Immediate Assessment and Stabilization
Identify and Treat the Underlying Cause
- Reassess the etiology of AKI immediately, as most cases are multifactorial and secondary to conditions like sepsis, shock, or volume depletion 2
- Evaluate for reversible causes including hypovolemia, obstruction (via renal ultrasound), and nephrotoxic exposures 1, 3
- In select cases requiring subspecialist expertise, consider evaluation for rare causes such as tumor lysis syndrome, thrombotic thrombocytopenic purpura, or cholesterol embolization syndrome 2
Fluid Management
- Use isotonic crystalloids (not colloids) for initial volume resuscitation 1, 4
- Balanced crystalloids (lactated Ringer's) are preferable to 0.9% saline due to emerging evidence of fewer adverse kidney outcomes 1, 2
- Fluid administration must be guided by hemodynamic assessment and reassessed frequently to avoid volume overload, which is associated with worse outcomes 1, 4
- In cirrhotic patients with AKI, consider albumin at 1 g/kg (maximum 100 g/day) after discontinuing diuretics 1
Critical pitfall: Volume overload in AKI is strongly associated with adverse outcomes and mortality 4. Avoid the vicious cycle of inappropriate fluid administration attempting to "reverse" established AKI, which leads to fluid overload 2
Medication Management
- Discontinue ALL nephrotoxic medications immediately: NSAIDs, ACE inhibitors, ARBs, aminoglycosides, vancomycin 5, 1
- Hold diuretics unless volume overload is present 1
- Adjust ALL medication doses for current GFR (not baseline renal function) 5, 6
- In cirrhotic patients, consider temporarily discontinuing beta-blockers 1
Hemodynamic Optimization
- Optimize hemodynamic status and kidney perfusion through appropriate use of fluids and vasopressors when indicated 2, 1
- Blood pressure targets are often higher in AKI patients 7
- Reassess volume and hemodynamic status daily, as optimization is critical for AKI resolution 2, 1
Monitoring Requirements
Daily Assessment
- Monitor serum creatinine daily until stabilization 5, 1
- Monitor urine output hourly in critically ill patients 1
- Assess fluid status regularly to avoid both hypovolemia and fluid overload 1
- Evaluate for complications including hyperkalemia, metabolic acidosis, and uremic symptoms 2, 5
Enhanced Monitoring for High-Risk Patients
- Patients with pre-existing CKD, heart failure, cirrhosis, or malignancy require more intensive monitoring 1
- "Stuttering recovery pattern" (fluctuating creatinine) is associated with worse mortality compared to prompt recovery and requires close observation 5, 2
Indications for Nephrology Consultation
Consult nephrology immediately for: 5, 1, 8
- Stage 2 or 3 AKI (creatinine ≥2.0× baseline)
- Persistent AKI despite initial management
- Severe electrolyte abnormalities or refractory hyperkalemia
- Severe metabolic acidosis
- Uremic symptoms (encephalopathy, pericarditis, pleuritis)
- Consideration for renal replacement therapy
- Unclear etiology requiring subspecialist expertise
Renal Replacement Therapy (RRT)
Absolute Indications for Urgent RRT
- Uremic encephalopathy (absolute indication)
- Refractory volume overload with pulmonary edema
- Severe metabolic acidosis refractory to medical management
- Hyperkalemia refractory to medical management
- Uremic pericarditis or pleuritis
- Certain toxin removal
RRT Timing Considerations
- The optimal timing of RRT initiation remains controversial, with studies not consistently demonstrating benefit to early-start dialysis 7, 4
- The decision for RRT should be individualized based on clinical context, overall patient condition, and presence of absolute indications 1, 2
- Early nephrology involvement is recommended for potential RRT planning 1
Important caveat: For controlled intravenous infusion of furosemide in high-dose parenteral therapy, an infusion rate not exceeding 4 mg/minute should be used in adults 9
Post-AKI Care and Follow-Up
Short-Term Follow-Up
- Follow-up renal function assessment at 1-2 weeks post-discharge for Stage 2-3 AKI 5, 8
- Reassess at 3 months to evaluate for CKD development in all AKI patients 5, 1, 8
- The severity of AKI determines the frequency and intensity of follow-up care 1
Long-Term Implications
- AKI is NOT a self-limited process but increases risk for future CKD, cardiovascular disease, and mortality even after apparent recovery 1, 4, 2
- Patients with residual renal damage should be managed according to CKD guidelines 1
- Continue avoiding nephrotoxic medications and maintain appropriate hydration after AKI episodes 1
Special Populations
Cirrhotic Patients
- AKI in cirrhosis may progress to hepatorenal syndrome requiring vasoconstrictors plus albumin 1
- Initiate furosemide therapy in the hospital setting for cirrhotic patients with ascites 9
- Sudden alterations in fluid and electrolyte balance may precipitate hepatic coma; strict observation is necessary during diuresis 9
Pediatric Considerations
- In premature neonates with respiratory distress syndrome, furosemide in the first weeks of life may increase risk of persistent patent ductus arteriosus 9
- Premature infants with post-conceptual age <31 weeks receiving furosemide doses >1 mg/kg/24 hours may develop toxic plasma levels including ototoxicity 9
Key Principles Summary
There are currently no targeted pharmacotherapies approved specifically for treating AKI itself 7, 4. Management remains supportive and focused on: