Also called tubulointerstitial nephritis. Acute interstitial renal inflammation. Pyuria (classically eosinophils) and azotemia occurring after administration of drugs that act as haptens, inducing hypersensitivity (eg, diuretics, NSAIDs, penicillin derivatives, proton pump inhibitors, rifampin, quinolones, sulfonamides).

Less commonly may be 2° to other processes such as systemic infections (eg, Mycoplasma) or systemic inflammatory disorders (eg, Sjögren syndrome, SLE, sarcoidosis).

Associated with fever, rash, pyuria, hematuria, and costovertebral angle tenderness, but can be asymptomatic. Remember the causes of inflammation to your DRAINS: ƒ Diuretics ƒ Rifampin ƒ Antibiotics (penicillins and cephalosporins) ƒ Proton pump Inhibitors ƒ NSAIDs ƒ Sulfa drugs

Acute (Allergic) Interstitial Nephritis

a form of acute renal failure; damage the tubules on idiosyncratic (idiopathic) basis

Antibodies and eosinophils attack the cells lining the tubules as a reaction to

• drugs (70%) - most commonly Penicillins, cephalosporins and Sulfa drugs including diuretics
• infection, and
• autoimmune disorders

Presentation:

• Acute renal failure *AIN should always be considered in patients with non-oliguric AKI
• Fever (80%)
• Rash (50%)
• Arthralgias
• Eosinophilia and eosinophiluria (80%)

Dx

elevated BUN:Cr with ratio below 20:1

Sterile pyuria: WBC and RBCs in the urine (NO eosinophils in the urine with AKI from NSAIDs)

In NSAID-induced AIN, renal biopsy would show minimal changes and a typical interstitial inflammatory pattern.