What is the best approach to treat a patient with acute kidney injury?

Treatment of Acute Kidney Injury

The cornerstone of AKI treatment is immediately identifying and reversing the underlying cause while discontinuing all nephrotoxic medications—this takes absolute priority over all other interventions. 1

Immediate Medication Management

Stop all nephrotoxic drugs immediately, including: 1

• NSAIDs
• Aminoglycosides
• ACE inhibitors and ARBs
• Diuretics (unless managing volume overload after adequate perfusion restored)
• Beta-blockers (especially in cirrhotic patients)
• Iodinated contrast media

The "triple whammy" combination (NSAIDs + diuretics + ACE inhibitors/ARBs) is particularly dangerous and must be discontinued immediately, as it more than doubles AKI risk. 1, 2 Each additional nephrotoxic agent increases AKI odds by 53%. 1

Adjust all remaining medication dosages based on reduced GFR and reassess frequently as kidney function changes. 2, 3

Fluid Resuscitation Strategy

Use isotonic crystalloids as first-line therapy for volume expansion, preferentially choosing balanced crystalloids (lactated Ringer's) over 0.9% saline to prevent metabolic acidosis and hyperchloremia. 1, 3

Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion. 1, 3

Avoid hydroxyethyl starches completely—they increase the risk of worsening AKI. 1, 4

Use dynamic indices (passive leg-raising test, pulse/stroke volume variation) rather than static measurements to guide fluid therapy. 1

Critical caveat: Avoid excessive fluid administration that leads to volume overload, as fluid overload >10-15% body weight is associated with adverse outcomes. 1 Consider earlier use of vasoactive medications instead of excessive fluid for hypotension. 1, 3

Hemodynamic Support

If fluid resuscitation fails to restore adequate blood pressure, use norepinephrine as first-line vasopressor. 1

Monitor volume status through clinical examination, echocardiography, or CVP when indicated to prevent fluid overload. 1

Special Population: Cirrhotic Patients

For cirrhotic patients with AKI, the approach differs significantly: 1, 3

• Discontinue both diuretics AND beta-blockers (not just diuretics)
• Administer IV albumin 1 g/kg bodyweight (maximum 100g) for two consecutive days to differentiate prerenal AKI from hepatorenal syndrome
• Initiate vasoconstrictors and albumin earlier in hepatorenal syndrome-AKI, as higher creatinine at treatment initiation leads to lower response rates
• Perform diagnostic paracentesis to evaluate for spontaneous bacterial peritonitis

Monitoring Protocol

Measure serum creatinine and electrolytes every 12-24 hours during acute management (every 4-6 hours initially for severe AKI). 1, 2

Track strict input/output measurements and monitor for signs of fluid overload (peripheral edema, pulmonary congestion, weight gain). 2, 3

Monitor urine output closely—oliguria is associated with poor prognosis. 2

Renal Replacement Therapy Indications

Consider RRT for persistent AKI despite appropriate interventions, based on clinical status rather than specific creatinine or BUN thresholds. 1, 3

Urgent RRT indications include: 2, 3

• Refractory hyperkalemia
• Severe metabolic acidosis
• Uremic encephalopathy, pericarditis, or pleuritis
• Severe oliguria unresponsive to fluid resuscitation
• Volume overload refractory to diuretics

Reassess need for continued RRT daily. 2, 3

What Does NOT Work (High-Quality Evidence)

Do not use the following interventions—they are ineffective based on level 1A/B evidence: 1

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

Critical Pitfalls to Avoid

Never use furosemide in hemodynamically unstable patients with prerenal AKI—it worsens volume depletion and reduces renal perfusion. 1

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, 2

Do not delay RRT when clear indications exist—this increases mortality. 2, 3

Avoid overly rapid correction of hyponatremia, which can lead to osmotic demyelination syndrome. 2, 3

Do not continue nephrotoxic medications during AKI recovery phase. 2

Diagnostic Workup

Perform urinalysis to detect hematuria, proteinuria, or abnormal urinary sediment to exclude structural renal diseases. 2, 3

Obtain kidney ultrasound immediately to rule out obstructive uropathy, particularly in older men with prostatic hypertrophy. 2, 3, 5

Assess for infections and gastrointestinal bleeding as precipitating causes. 2

Follow-Up Strategy

Evaluate renal function within 3-7 days after last RRT session. 3

Perform follow-up at 3 months after AKI to assess resolution or progression to chronic kidney disease. 3

Target follow-up to high-risk populations, including individuals with baseline CKD, as even patients with complete recovery remain at increased risk of progressive CKD. 1

Consider nephrology referral for severe AKI (stage 3), inadequate response to supportive treatment, or risk factors for progression to chronic kidney disease. 3, 6