Treatment of Acute Kidney Injury
The cornerstone of AKI treatment is immediately discontinuing all nephrotoxic medications while simultaneously identifying and reversing the underlying cause—this takes priority over all other interventions. 1
Immediate Medication Management
Stop all nephrotoxic drugs immediately, including: 1
- NSAIDs
- Aminoglycosides
- ACE inhibitors and ARBs
- Diuretics
- Beta-blockers
- Vasodilators
- Iodinated contrast media
The "triple whammy" combination (NSAIDs + diuretics + ACE inhibitors/ARBs) is particularly dangerous and must be discontinued immediately. 1 Each additional nephrotoxin increases AKI odds by 53%, so avoid combining multiple nephrotoxic agents. 1
Critical Pitfall
Never 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. 2
Fluid Resuscitation and Hemodynamic Optimization
Use isotonic crystalloids as first-line therapy for volume expansion in hypovolemic patients with prerenal AKI. 1, 2
Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion. 1, 2
Avoid hydroxyethyl starches—they increase the risk of worsening AKI. 1
Use dynamic indices (passive leg-raising test, pulse/stroke volume variation) rather than static measurements to guide fluid therapy. 1
Vasopressor Therapy
If fluid resuscitation fails to restore adequate blood pressure, initiate vasopressor therapy rather than continuing excessive fluid administration. 2 Norepinephrine is preferred over dopamine. 3
Monitoring for Fluid Overload
Monitor closely using: 1
- Urine output
- Vital signs
- Echocardiography or CVP when indicated
Volume overload worsens AKI outcomes, so pay careful attention to overall fluid balance. 4
Special Population: Cirrhotic Patients
In cirrhotic patients with AKI, discontinue both diuretics AND beta-blockers (not just diuretics). 1, 3
Administer IV albumin 1 g/kg bodyweight (maximum 100g) for two consecutive days to differentiate prerenal AKI from other causes and for therapeutic benefit. 1, 2
For hepatorenal syndrome AKI (HRS-AKI) not responding to volume expansion, administer vasoconstrictors (terlipressin, norepinephrine, or midodrine plus octreotide) along with albumin. 2, 3
Monitoring During Acute Management
Measure serum creatinine and electrolytes every 12-24 hours during acute management. 1, 2
Monitor closely in the first 48-72 hours, focusing on: 1, 2
- Urine output
- Vital signs
- Fluid balance
- Electrolyte disturbances (particularly hyperkalemia)
- Metabolic acidosis
Critical Pitfall
Do not use eGFR equations designed for CKD to assess renal function in AKI—they are inaccurate in this setting. 1, 2
Renal Replacement Therapy
Consider RRT based on the patient's overall clinical condition rather than specific creatinine or BUN thresholds. 1, 3
Indications for RRT include: 3, 5
- Refractory hyperkalemia
- Volume overload unresponsive to diuretics
- Intractable metabolic acidosis
- Uremic complications (encephalopathy, pericarditis, pleuritis)
- Toxin removal
Recent studies have not demonstrated consistent benefit to early-start dialysis, so timing should be individualized based on clinical status. 6, 4
Management Algorithm by AKI Stage
Stage 1 AKI: 2
- Remove nephrotoxic medications
- Provide volume expansion if hypovolemic
- Monitor renal function closely
- All Stage 1 interventions
- Consider vasopressor therapy if fluid resuscitation fails
- Consider nephrology consultation
- Prepare for potential RRT
Recovery Phase Management
Continue nephrotoxin avoidance during the recovery phase to prevent re-injury. 2, 3
Educate patients to avoid NSAIDs or new medications without consulting their healthcare provider. 3
Reassess etiology and consider nephrology consultation for persistent AKI (>48 hours). 2