Treatment of Acute Kidney Injury
Immediately discontinue all nephrotoxic medications and identify the underlying cause—this takes priority over all other interventions. 1, 2
Immediate Medication Management
Stop these medications immediately:
- NSAIDs (including over-the-counter)
- ACE inhibitors and ARBs
- Diuretics
- Beta-blockers
- Aminoglycosides
- Iodinated contrast media 1, 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%, and combining multiple agents more than doubles the risk. 3, 1
Fluid Resuscitation Strategy
Use isotonic crystalloids (preferably lactated Ringer's over 0.9% saline) as first-line therapy for volume expansion. 1, 2 Lactated Ringer's prevents metabolic acidosis and hyperchloremia associated with normal saline. 3
Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion. 1, 2
Avoid hydroxyethyl starches completely—they increase AKI risk and mortality. 3, 1
Fluid Administration Approach:
- Base fluid administration on repeated hemodynamic assessment using dynamic indices (passive leg-raising test, pulse/stroke volume variation) rather than static measurements 3, 1
- Consider earlier use of vasopressors instead of excessive fluid administration for hypotension 3
- Avoid fluid overload >10-15% body weight, which is associated with adverse outcomes 3
Critical pitfall: Do not use furosemide in hemodynamically unstable patients with prerenal AKI—it worsens volume depletion and reduces renal perfusion. 1 Diuretics should only be used for managing volume overload after adequate renal perfusion is restored. 1
Vasopressor Therapy
Use norepinephrine as the first-line vasopressor over dopamine. 2 Dopamine should not be used to prevent or treat AKI. 3, 2
Special Population: Cirrhotic Patients
In cirrhotic patients with AKI, discontinue BOTH diuretics AND beta-blockers (not just diuretics). 1, 2
Administer IV albumin 1 g/kg bodyweight (maximum 100g) for two consecutive days to differentiate prerenal AKI from hepatorenal syndrome. 1, 2 If serum creatinine remains elevated despite this intervention, add vasoactive agents (terlipressin, norepinephrine, or midodrine plus octreotide) along with continued albumin. 2
Monitoring Protocol
Measure 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
Use echocardiography or CVP when indicated to assess volume status and prevent fluid overload. 1, 2
Do not use eGFR equations (MDRD, CKD-EPI) to assess renal function in AKI—they require steady-state creatinine and are inaccurate in acute settings. 1
Renal Replacement Therapy
Individualize timing of RRT based on overall clinical condition rather than specific creatinine or BUN thresholds. 1, 2 Consider RRT for:
- Refractory hyperkalemia
- Intractable metabolic acidosis
- Persistent volume overload despite appropriate interventions
- Uremic complications 2
What Does NOT Work (Avoid These)
Do not use these interventions—they have no benefit or cause harm:
- Dopamine for AKI prevention or treatment 3, 2
- Diuretics to prevent or treat AKI (except for volume overload management) 3, 1
- N-acetylcysteine 2
- Recombinant human insulin-like growth factor 1 3, 2
Recovery Phase Management
Continue nephrotoxin avoidance during the recovery phase to prevent re-injury. 3, 2 Educate patients to avoid NSAIDs or new medications without consulting their healthcare provider. 3, 2
Target follow-up to high-risk populations: individuals with baseline CKD, severe AKI, or incomplete recovery at hospital discharge require monitoring for development or progression of chronic kidney disease. 3, 2