Diagnosing drug-induced AIN in the hospitalized patient: a challenge for the clinician

Abstract

Drug-induced acute interstitial nephritis (AIN) is a relatively common cause of hospital-acquired acute kidney injury (AKI). While prerenal AKI and acute tubular necrosis (ATN) are the most common forms of AKI in the hospital, AIN is likely the next most common. Clinicians must differentiate the various causes of hospital-induced AKI; however, it is often difficult to distinguish AIN from ATN in such patients. While standardized criteria are now used to classify AKI into stages of severity, they do not permit differentiation of the various types of AKI. This is not a minor point, as these different AKI types often require different therapeutic interventions. Clinicians assess and differentiate AIN from these other AKI causes by utilizing clinical assessment, various imaging tests, and certain laboratory data. Gallium scintigraphy has been employed with mixed results. While a few serum tests, such as eosinophilia may be helpful, examination of the urine with tests such as dipstick urinalysis, urine chemistries, urine eosinophils, and urine microscopy are primarily utilized. Unfortunately, these tools are not always sufficient to definitively clinch the diagnosis, making it a challenging task for the clinician. As a result, kidney biopsy is often required to accurately diagnose AIN and guide management.

Figure 1. Prevalence of AIN in patients with acute kidney injury. AIN = acute interstitial nephritis.

Figure 2. Positron emission tomography (FDG-PET) scan in a patient with acute interstitial nephritis (AIN) in the setting of drug rash with eosinophilia and systemic symptoms (DRESS) syndrome.

Figure 3. White blood cell cast in the urine of a patient with acute interstitial nephritis (AIN).

Figure 4. Kidney biopsy of a patient with acute interstitial nephritis (AIN) highlighting the inflammatory interstitial infiltrate with prominent eosinophils.