From the Research
Serum BUN and creatinine increase in acute interstitial nephritis (AIN) because the inflammation damages the kidney's tubules and interstitium, impairing their ability to filter waste products from the blood. This kidney injury typically develops rapidly over days to weeks, with BUN and creatinine serving as important laboratory markers for diagnosing AIN. The pathogenesis of AIN involves antigen-initiated cell-mediated injury, with drugs accounting for 70% of all cases, and the remaining cases due to infections, autoimmune diseases, and rarely idiopathic 1. The central component of renal injury in AIN is altered tubular function, which usually precedes decrements in filtration rate, and the key to early diagnosis is vigilance for the presence of tubular dysfunction in non-oliguric individuals, especially in patients with modest but gradual increments in creatinine level 1. The most recent and highest quality study suggests that early withdrawal of the culprit drug together with corticosteroid therapy remain the mainstay of treatment, although recent studies have shown that prolonged treatment beyond 8 weeks does not further improve kidney function recovery 2. Some of the key points to consider in the management of AIN include:
- Early recognition and elimination of the offending source of antigen
- Use of a limited course of steroid therapy where indicated
- Monitoring of serum creatinine and other laboratory markers to assess response to treatment
- Consideration of kidney biopsy to provide a definitive diagnosis and guide treatment decisions
- Awareness of the potential for AIN to be caused by a wide range of medications, including antibiotics, NSAIDs, and proton pump inhibitors, as well as infections, autoimmune disorders, and systemic diseases. Overall, the management of AIN requires a comprehensive approach that takes into account the underlying cause of the disease, the severity of the kidney injury, and the individual patient's needs and circumstances.