What is the management plan for a patient with Rheumatoid Arthritis (RA) who develops Acute Kidney Injury (AKI) with impaired renal function, as evidenced by elevated creatinine and severely reduced urine output, while taking naproxen (Nonsteroidal Anti-Inflammatory Drug (NSAID)) and paracetamol (Acetaminophen)?

Management of NSAID-Induced AKI in ICU Setting

Stop naproxen immediately—this is the single most critical intervention for this patient with severe AKI (Cr 200, urine output 50ml/24h) as NSAIDs are directly nephrotoxic and continuation will prevent recovery. 1, 2

Immediate Actions Required

1. Discontinue All Nephrotoxins

• Stop naproxen immediately as it is contraindicated in patients with moderate to severe renal impairment (creatinine clearance <30 mL/min), and this patient clearly meets criteria for severe AKI 2
• Discontinue paracetamol temporarily during the acute phase 1
• Review and stop any other nephrotoxic medications including ACE inhibitors, ARBs, diuretics if present 3, 1
• NSAIDs account for 20-25% of AKI cases in critically ill patients, and combining multiple nephrotoxins more than doubles AKI risk 1, 4

2. Assess Volume Status and Resuscitate

• Immediately assess for volume depletion or overload 1
• If hypovolemic, initiate aggressive intravenous fluid resuscitation 1
• Place bladder catheter to monitor hourly urine output given severe oliguria (50ml/24h) 1, 4
• Correct any volume abnormalities before considering dialysis 1

3. Evaluate for Dialysis Indications

This patient likely requires urgent dialysis given:

• Severe oliguria (<100ml/24h indicates Stage 3 AKI) 3
• Elevated creatinine (200 μmol/L ≈ 2.3 mg/dL suggests significant dysfunction)
• Monitor for absolute indications: hyperkalemia, severe metabolic acidosis, uremic symptoms, or volume overload refractory to diuretics 1

4. Do NOT Use Dopamine

• Dopamine is not recommended for prevention or treatment of AKI 1
• No evidence supports dopamine for renal protection in AKI
• Focus instead on volume optimization and nephrotoxin removal

Monitoring Protocol

Laboratory Surveillance

• Daily serum creatinine and eGFR during acute phase 1
• Daily to twice-daily electrolytes, especially potassium given risk of hyperkalemia with oliguria 1
• Monitor for metabolic acidosis
• Check urinalysis to differentiate AKI etiology (look for eosinophils suggesting acute interstitial nephritis from NSAIDs) 3

Clinical Monitoring

• Hourly urine output via bladder catheter 1, 4
• Daily weights and fluid balance
• Blood pressure monitoring (NSAIDs can worsen hypertension) 2, 5
• Watch for signs of volume overload or uremic symptoms

Pathophysiology Context

NSAIDs cause AKI through multiple mechanisms:

• Prostaglandin inhibition leading to afferent arteriolar vasoconstriction and reduced renal blood flow 6, 7
• Acute interstitial nephritis (occurs in 80-90% of NSAID-related renal biopsies) 3
• Acute tubular necrosis from ischemia 3
• Risk factors include ICU setting, concurrent medications, and underlying RA 3

Recovery Expectations

• NSAID-induced AKI is usually reversible after drug discontinuation 8, 9, 7
• Recovery typically occurs over days to weeks (mean 37 days in one series) 8
• Serum creatinine should begin improving within 3-7 days after stopping naproxen 8, 9
• Some patients may require temporary dialysis but most recover full renal function 8, 9

Critical Pitfalls to Avoid

• Never continue NSAIDs in established AKI—this is the most common preventable error 1, 2
• Do not use dopamine for "renal protection"—this is ineffective and outdated 1
• Avoid combining multiple nephrotoxins during recovery phase 1
• Do not delay dialysis if absolute indications present (life-threatening hyperkalemia, severe acidosis, uremic pericarditis) 1

Alternative Pain Management for RA

Once renal function stabilizes:

• Consider topical NSAIDs for localized joint pain 5
• Use acetaminophen at appropriate doses (though temporarily held now) 5
• Non-pharmacological therapies 5
• Avoid systemic NSAIDs long-term in this patient given demonstrated susceptibility to nephrotoxicity 2, 6