Acute interstitial nephritis (AIN) is a significant cause of acute kidney injury, representing 15-27% of renal biopsies conducted for this condition. Drug-induced AIN is the most prevalent type, frequently linked to antimicrobials and NSAIDs.
The pathogenesis involves an immune response to either endogenous or exogenous antigens processed by tubular cells, primarily driven by cell-mediated immunity. The characteristic inflammation involves lymphocytes, macrophages, eosinophils, and plasma cells, eventually leading to interstitial fibrosis. While many cases are minimally symptomatic, the presence of fever, skin rash, arthralgias, and peripheral eosinophilia are important diagnostic clues.
Treatment centers on identifying and removing the causative drug. Recent research suggests that early steroid treatment (within 7 days of diagnosis) enhances renal function recovery and reduces chronic kidney impairment risk. Delayed steroid treatment is less effective once fibrosis develops.
Acute interstitial nephritis (AIN) represents a frequent cause of acute kidney injury, accounting for 15-27% of renal biopsies performed because of this condition. By and large, drug-induced AIN is currently the commonest etiology of AIN, with antimicrobials and nonsteroidal anti-inflammatory drugs being the most frequent offending agents. Pathogenesis is based on an immunologic reaction against endogenous nephritogenic antigens or exogenous antigens processed by tubular cells, with cell-mediated immunity having a major pathogenic role. The characteristic interstitial infiltrates, mostly composed of lymphocytes, macrophages, eosinophils, and plasma cells, experience a rapid transformation into areas of interstitial fibrosis. A significant proportion of AIN has nowadays an oligosymptomatic presentation, although the presence of specific extrarenal symptoms such as fever, skin rash, arthralgias, and peripheral eosinophilia has an important role to orientate clinical diagnosis. Identification and removal of the offending drug are the mainstay of the treatment, but recent studies strongly suggest that early steroid administration (within 7 days after diagnosis) improves the recovery of renal function, decreasing the risk of chronic renal impairment. Delayed steroid treatment, when interstitial fibrosis has taken place, would have a less pronounced or nule therapeutic benefit.
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