Discontinue Pantoprazole Immediately
The best next step is to discontinue pantoprazole (Option B), as this patient has developed acute tubulointerstitial nephritis (AIN), a well-documented adverse effect of proton pump inhibitors that requires immediate drug cessation.
Clinical Reasoning
This patient presents with classic features of PPI-induced acute interstitial nephritis:
- Acute kidney injury: Serum creatinine rose from 0.90 mg/dL to 2.10 mg/dL (eGFR 34 mL/min/1.73 m²) over 4 days 1
- Urinary findings: WBC casts (2/lpf) and pyuria (10 WBCs/hpf) are pathognomonic for interstitial nephritis 1, 2
- Peripheral eosinophilia: Elevated eosinophils at 8% (normal 0-3%) suggests drug hypersensitivity 2
- Temporal relationship: Pantoprazole was started "a few days before admission" and continued throughout hospitalization 1, 2
- Systemic symptoms: Malaise without other localizing symptoms is consistent with drug-induced AIN 1, 3
Why Discontinue Pantoprazole
The FDA label explicitly states: "Acute tubulointerstitial nephritis (TIN) has been observed in patients taking PPIs and may occur at any point during PPI therapy. Patients may present with varying signs and symptoms from symptomatic hypersensitivity reactions to non-specific symptoms of decreased renal function (e.g., malaise, nausea, anorexia)... Discontinue pantoprazole sodium and evaluate patients with suspected acute TIN" 1.
- PPI-induced AIN can occur at any time during therapy, typically within weeks to months of initiation 1, 2, 3
- Case reports document pantoprazole-induced AIN presenting with elevated creatinine, oliguria, fever, and eosinophiluria 2, 3
- Early detection and prompt discontinuation prevent progression to acute renal insufficiency 2
- One documented case showed creatinine rising from 1.0 to 6.1 mg/dL within days of pantoprazole re-exposure 2
Why Not the Other Options
Option A (Empirical antibiotics): This patient has no fever (37.7°C is normal), no dysuria, no systemic signs of infection, and the urinalysis shows WBC casts—not bacteria or nitrites—which points to interstitial inflammation rather than pyelonephritis 1, 2.
Option C (Renal ultrasonography): While imaging may eventually be needed, it will not change immediate management. The urinalysis findings (WBC casts, eosinophilia) already establish the diagnosis of AIN, making obstruction or structural abnormalities unlikely 2, 3.
Option D (IV fluid bolus): The patient is hemodynamically stable (BP 120/76, moist mucous membranes) without evidence of volume depletion. Fluid administration will not reverse drug-induced AIN and may delay the critical intervention of stopping the offending agent 1, 2.
Management After Discontinuation
Following pantoprazole cessation:
- Corticosteroid therapy: Prednisone 40-60 mg/day (1 mg/kg/day) should be considered, as corticosteroids may facilitate recovery of renal function in drug-induced AIN 2, 3
- Monitor renal function: Serial creatinine measurements every 2-4 days to assess response 2
- Renal biopsy: Consider if diagnosis remains uncertain or renal function fails to improve within 3-7 days of drug discontinuation 2, 3
- Alternative GERD management: The patient has diet-controlled diabetes and no active GERD symptoms; pantoprazole may not be necessary at all 1
Common Pitfalls to Avoid
- Do not continue pantoprazole while pursuing other diagnostic workup—every additional dose increases renal injury 1, 2
- Do not assume infection based solely on pyuria and leukocytosis; WBC casts distinguish AIN from UTI 2, 3
- Do not delay intervention waiting for biopsy confirmation; clinical diagnosis with prompt drug cessation is appropriate 2
- Do not restart pantoprazole after recovery, as re-challenge can cause rapid recurrence of AIN 2
The Naranjo probability scale in documented cases suggests a "highly probable relationship" between pantoprazole and AIN when temporal association, urinary eosinophils, and improvement after discontinuation are present 2.