Tubulointerstitial Disease — DCE Clinical Case

Reading the data — what each piece contributes

• Urine microscopy: sterile pyuria with white-cell casts localises inflammation to the renal tubulointerstitium — the most telling bedside clue in AIN — while modest sub-nephrotic proteinuria fits a tubular rather than glomerular process ^{[1] [2]}.
• Urinary eosinophils at 3%: supportive but weak. The test performs poorly as a discriminator — eosinophiluria occurs in cystitis, pyelonephritis and other AKI causes, and biopsy-proven series show limited sensitivity and specificity — so it raises probability without deciding anything ^{[2] [3]}.
• The drug chart: two plausible culprits with different signatures. The amoxicillin course (completed six weeks ago) fits the classic antibiotic latency of days to weeks; the pantoprazole (seven months) fits the PPI pattern — long silent latency, no allergic features, discovered late ^{[4] [1]}. Ibuprofen PRN is a third possibility and the one class that can add nephrotic-range proteinuria — his 0.7 g/day argues against a dominant NSAID lesion ^[1].
• Normal ultrasound and absent triad: normal kidney size supports an acute process; the missing rash, fever and eosinophilia exclude nothing — the full triad appears in only a small minority of modern drug-induced AIN ^[2].