What is the most appropriate treatment for a patient with intrinsic acute kidney injury likely caused by amoxicillin (amoxicillin/clavulanate)?

Management of Intrinsic Acute Kidney Injury Due to Amoxicillin/Clavulanate

Discontinuation of amoxicillin/clavulanate is the most appropriate treatment for this patient with intrinsic acute kidney injury likely caused by this antibiotic.

Clinical Presentation Analysis

The patient presents with classic signs of drug-induced acute interstitial nephritis (AIN):

• Flank pain and dark urine
• Elevated creatinine (2.8 mg/dL) from previously normal baseline
• Urinalysis showing granular casts, WBCs, RBCs, and importantly, eosinophils
• FENa of 2.2% consistent with intrinsic renal injury
• Recent exposure to amoxicillin/clavulanate, a known nephrotoxic agent

Management Algorithm

1. Immediate discontinuation of the offending agent

   • Stop amoxicillin/clavulanate immediately
   • Consider alternative antibiotic therapy for sinus infection if still needed

2. Supportive care

   • Maintain adequate hydration
   • Monitor fluid status and electrolytes
   • Avoid additional nephrotoxic medications

3. Monitoring

   • Daily assessment of renal function (BUN, creatinine)
   • Monitor urine output
   • Electrolyte monitoring

4. Indications for nephrology consultation

   • Worsening renal function despite drug discontinuation
   • Severe electrolyte abnormalities
   • Uremic symptoms
   • Need for renal replacement therapy

Evidence Supporting Discontinuation of Amoxicillin/Clavulanate

Amoxicillin and amoxicillin/clavulanate are well-documented causes of acute kidney injury through several mechanisms:

1. Acute interstitial nephritis (AIN): The presence of eosinophils in urine is highly suggestive of drug-induced AIN 1, 2, 3. This is an immune-mediated hypersensitivity reaction that typically resolves with discontinuation of the offending agent.

2. Crystal nephropathy: High-dose amoxicillin can cause crystalluria and tubular obstruction 4. The patient's dark urine and granular casts could be consistent with this mechanism.

Why Other Options Are Not Appropriate

1. Urgent kidney replacement therapy: Not indicated as the patient is clinically stable with no signs of uremic emergency, severe hyperkalemia, or volume overload. Renal function typically recovers after discontinuation of the offending agent 1, 2.

2. Furosemide 80 mg IV twice daily: Loop diuretics are not indicated in drug-induced AIN and could potentially worsen kidney injury by decreasing renal perfusion.

3. IV 5% dextrose at 100 mL/hr: While hydration is important, a specific fluid prescription without addressing the underlying cause (the nephrotoxic drug) is insufficient.

Monitoring After Discontinuation

• Daily BUN and creatinine until improvement begins
• Monitor urine output
• Assess for signs of recovery (decreased flank pain, lightening of urine color)
• Expect gradual improvement in renal function over days to weeks

Potential Pitfalls

1. Failure to recognize drug-induced nephrotoxicity: Always consider medications as potential causes of acute kidney injury, especially antibiotics.

2. Delayed discontinuation: Continued exposure to the nephrotoxic agent will prolong and potentially worsen kidney injury.

3. Misattribution to other causes: The presence of eosinophils in urine is a key finding suggesting drug-induced AIN rather than other causes of AKI.

4. Restarting the offending agent: Amoxicillin/clavulanate should be added to the patient's allergy list to prevent future exposure.

The patient's presentation is classic for drug-induced AIN, and prompt discontinuation of the offending agent is the cornerstone of management to prevent further kidney damage and allow recovery of renal function.