Definition
Acute tubulointerstitial nephritis (ATIN) is an acute inflammation of the renal interstitium and tubules that causes a decline in renal function over a period of days to weeks.
Etiology
Medications (most common)
- Antibiotics: β-lactams, sulfonamides, rifampin, fluoroquinolones
- NSAIDs
- Proton pump inhibitors and H2 blockers
- Loop diuretics and thiazides
- Anticonvulsants: phenytoin, valproate, carbamazepine, phenobarbital
- Other: allopurinol
Pathophysiology
- Immune-mediated tubulointerstitial damage (allergic interstitial nephritis) is the most widely accepted theory.
- Inflammatory infiltrates → tissue edema and tubular cell damage → compromised tubular flow
- Allergic interstitial nephritis: drugs act as haptens → type IV hypersensitivity reaction
- Acute obstruction: crystals (from e.g., uric acid, medications) or proteins (e.g., light chains) obstruct tubules
Clinical features
- Onset is typically 7-10 days after starting the offending drug.
- Classic Triad (present in only 10-15% of pts):
- Fever
- Rash (maculopapular)
- Arthralgias
- Features of Acute Kidney Injury (AKI): Oliguria, ↑ BUN, ↑ Cr.
Diagnostics
- Labs:
- Peripheral eosinophilia.
- ↑ BUN and ↑ serum Cr.
- Urinalysis (UA):
- WBC casts (pathognomonic but not always present).
- Sterile pyuria (WBCs in urine without bacteriuria).
- Eosinophiluria (seen with Wright or Hansel stain; highly specific but not sensitive).
- Mild proteinuria.
- Renal Biopsy (definitive Dx, but not always required):
- Interstitial inflammatory infiltrate (lymphocytes, macrophages, eosinophils).
Tip
Although frequently cited as a diagnostic clue, in clinical practice, urine eosinophils lack sensitivity and specificity for reliably confirming ATIN.