From the Research
The BUN/creatinine ratio increases in acute interstitial nephritis (AIN) primarily due to the differential effects of the inflammatory process on kidney function, as evidenced by the most recent study in 2024 1. In AIN, there is inflammation of the renal interstitium, which affects the tubules more than the glomeruli initially. This tubular dysfunction leads to decreased reabsorption of urea (measured as blood urea nitrogen or BUN), while creatinine excretion remains relatively preserved in early stages. As a result, BUN levels rise disproportionately compared to creatinine, increasing the BUN/creatinine ratio above the normal range of 10-20:1.
Some key points to consider in AIN include:
- The inflammatory process can cause reduced renal blood flow, which further enhances urea reabsorption while having less effect on creatinine clearance 2.
- Other factors that may contribute to this elevated ratio include volume depletion from fever or reduced oral intake during illness, and the catabolic state induced by the inflammatory process itself, which increases protein breakdown and urea production 3.
- The clinical presentation of AIN can vary, with some cases being oligosymptomatic, while others may present with fever, skin rash, arthralgias, and peripheral eosinophilia 4.
- Early withdrawal of the culprit drug and corticosteroid therapy remain the mainstay of treatment for AIN, although the effectiveness of corticosteroids may depend on the timing of administration and the underlying cause of AIN 5, 3.
Overall, the increase in BUN/creatinine ratio in AIN is a result of the complex interplay between the inflammatory process, tubular dysfunction, and reduced renal blood flow, and requires careful consideration of the underlying cause and clinical presentation to guide treatment.