Interstitial Nephritis

Aka, tubulointerstitial nephritis when the tubules are also involved. Renal interstitium supports the tubules, produces hormones, and helps regulate fluid and electrolyte balance. Medications, infections, autoimmune disorders, and specific genes can cause inflammation in the interstitium. Inflammatory cells infiltrate the renal interstitium and impair tubular functioning and reduce GFR. Medications: Interstitial nephritis is most commonly caused by allergic drug reactions to drugs: NSAIDs, beta-lactams, diuretics, proton pump inhibitors, anti-cancer drugs, and several others. These drugs act as haptens and bind to tubular cell components and trigger an immune response (in other words, they cause hypersensitivity reactions). Be aware that interstitial nephritis is apparent 1-3 weeks after most medications, but the timeframe varies by drug. Infections & other disorders including Legionella, CMV, Streptococcus (plus several others); Sarcoidosis and SLE. The "classic triad" of signs and symptoms consists of rash, fever, and eosinophilia; however, it's rare to see all three manifestations at once, and patients may have pyuria or hematuria. Urine - sterile pyuria, eosinophiluria, white blood cell casts, and proteinuria; we can also look for characteristic histopathology after biopsy. Histopathology: Characterized by interstitial edema with white blood cell infiltration; granuloma formation is also possible. Note that the condition can become chronic, in which case we might see fibrosis, scarring, and atrophy. For more great histology samples and explanations, see: Renalfellow.org There's no specific treatment; remove the drug or treat the causative illness.