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For further information, see CMDT Part 24-07: Interstitial Nephritis
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Acute interstitial nephritis accounts for ∼10–15% of cases of intrinsic acute kidney injury (AKI)
Interstitial inflammatory response with edema is the typical pathologic finding; tubular damage may be present as well
Causes of acute interstitial nephritis
Drugs (> 70% of cases), including
Infectious diseases, including
Autoimmune disorders, including
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Fever (> 80%)
Rash (25–50%)
Arthralgias
Peripheral blood eosinophilia (80%)
The classic triad of fever, rash, and arthralgias is present in only 10–15% of cases
Differential diagnosis
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Peripheral blood eosinophilia (80%)
Acute or chronic kidney disease
Urine microscopy reveals white cells (70%), red cells (50%), and white cell casts (15%)
Proteinuria usually modest (< 2 g/d)
Kidney biopsy is sometimes needed
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Supportive measures
Prompt removal of the inciting agent
Corticosteroids
Consider giving if kidney injury persists despite removal of culprit drug
Efficacy is diminished if started more than 1–2 weeks after onset of AKI
For severe cases of drug-induced interstitial nephritis
Short-term, high-dose methylprednisolone (0.25–0.5 g/d intravenously for 1–4 days) or
Prednisone (60 mg/d orally for 4–6 weeks) followed by a taper can be used
Prognosis good; recovery occurs over weeks to months
Dialysis may be necessary in up to 33%
Patients rarely progress to end-stage kidney disease
Prognosis worse in those with prolonged courses of oliguric failure and advanced age