A Synopsis of AFP's "Diagnosis and Management of Acute Interstitial Nephritis"

Diagnosis and Management of Acute Interstitial Nephritis
CHARLES M. KODNER, M.D., and ARCHANA KUDRIMOTI, M.D. University of Louisville School of Medicine, Louisville, Kentucky
Am Fam Physician. 2003 Jun 15;67(12):2527-2534.
http://www.aafp.org/afp/2003/0615/p2527.pdf

     Acute interstitial nephritis (AIN) is acute renal failure with inflammation of the interstitium and renal tubules. AIN is due to one of three causes; drug-induced, infection, and immune/ neoplasia. There is a wide spectrum of drugs that can cause AIN, including antibiotics, NSAIDs, antivirals, omeprazole, sulfa drugs, ranitidine, captopril, furosemide, thiazides, and many, many more. The side effects may not appear for up to two weeks. It is also not dose dependent. Infections that cause AIN include acute bacterial pyelonephritis, renal TB, and fungal nephritis. Systemic infections can indirectly cause AIN by lowering cell mediated immunity (HIV, sarcoid, lead exposure). Immune disoirders responsible for AIN include sjogren's, SLE, and wegeners.
     AIN is caused when inflammatory cells invade the interstitium, leading to edema . Patchy or diffuse fibrosis will occur in the cortex and medullocortical junction. AIN presents with nonspecific features such as oliguria, anorexia, malaise, fever, rash, nausea and vomiting. The pathology varies widely depending on which drug has caused the problem.  Immune-induced AIN is due to granuloma formation with epithelioid giant cells.  Lab studies are generally nonspecific and variable. An elevated creatinine and BUN represent a rapid deterioration of renal function. The renal biopsy is the definitive diagnosis. A positive biopsy will show patchy plasma and lymphocytic infiltration in the peritubular area. Poor prognostic factors on biopsy include diffuse inflammation, neutrophilia, and excessive interstitial fibrosis.
    When AIN is suspected, the first step is to stop the offending medication. If this leads to clinical improvement, then the patient is managed with supportive care. If the patient does not show clinical improvement, then a biopsy can be done. If there is a contraindication to biopsy, a renal ultrasound or gallium scan can be considered. If the patient is positive for AIN on biopsy, and their is no fibrosis, steroids can be started. If the steroids do not improve renal function, then they can be discontinued and supportive therapy can be started. Supportive therapy includes fluid and electrolyte management, symptomatic relief of fever and rash, and avoiding dangerous drugs. Immunosuppressive therapy is another option if warranted. Uncontrolled hyperkalemia, azotemia, mental status changes, and fluid/ electrolyte issues are indications for dialysis.
     Most patients will recover in a weeks after discontinuing the medication. There is initial rapid phase of recovery lasting up to 8 weeks and a slow phase which may last up to a year.