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Background Acute interstitial nephritis (AIN) is characterized by an inflammatory infiltrate in the renal interstitium. The etiology of AIN is broad with the most common cause being medications. Treatment includes removal of the offending agent, glucocorticoid therapy, and immunosuppression. Rosehips are a fruit produced from wild roses that are often used in teas and herbal supplements. They are reported to have anti-inflammatory effects and sought after for this purported benefit. Case presentation We present a case of a 67-year-old woman who presented with acute kidney injury after two months of excessive rosehip tea consumption. She was dialyzed for 1 month and treated with oral steroids. Her initial renal biopsy revealed AIN, a thin glomerular basement membrane, and five nodular sclerosed glomeruli. Her work-up was negative for known causes of AIN and the etiology was determined to be rosehip tea. Two months after initial presentation she continued to have clinical and pathologic signs of AIN. She was started on mycophenolate mofetil (MMF) with clinical improvement. Conclusion Rosehip tea is known to have diuretic properties and, when consumed, may lead to a self-perpetuating cycle of intake. Excessive consumption may lead to increased concentrations of arachidonic acid and its metabolites. These metabolites have been shown to perpetuate an inflammatory response capable of causing AIN. Providers should be aware when counseling patients that excessive intake of rosehip tea may lead to AIN.
Background Acute interstitial nephritis (AIN) is characterized by an inflammatory infiltrate in the renal interstitium. The etiology of AIN is broad with the most common cause being medications. Treatment includes removal of the offending agent, glucocorticoid therapy, and immunosuppression. Rosehips are a fruit produced from wild roses that are often used in teas and herbal supplements. They are reported to have anti-inflammatory effects and sought after for this purported benefit. Case presentation We present a case of a 67-year-old woman who presented with acute kidney injury after two months of excessive rosehip tea consumption. She was dialyzed for 1 month and treated with oral steroids. Her initial renal biopsy revealed AIN, a thin glomerular basement membrane, and five nodular sclerosed glomeruli. Her work-up was negative for known causes of AIN and the etiology was determined to be rosehip tea. Two months after initial presentation she continued to have clinical and pathologic signs of AIN. She was started on mycophenolate mofetil (MMF) with clinical improvement. Conclusion Rosehip tea is known to have diuretic properties and, when consumed, may lead to a self-perpetuating cycle of intake. Excessive consumption may lead to increased concentrations of arachidonic acid and its metabolites. These metabolites have been shown to perpetuate an inflammatory response capable of causing AIN. Providers should be aware when counseling patients that excessive intake of rosehip tea may lead to AIN.
Background: Accurate diagnosis of acute tubulointerstitial nephritis (AIN) often requires a kidney biopsy. We previously developed a diagnostic statistical model for predicting biopsy-confirmed AIN by combining four laboratory tests after evaluating over 150 potential predictors from the electronic health record. Here, we validate this diagnostic model in two biopsy-based cohorts at Johns Hopkins Hospital (JHH) and Yale, which were geographically and temporally distinct from the development cohort, respectively. Methods: We analyzed patients who underwent kidney biopsy at JHH and Yale University (2019-2023). We assessed discrimination (AUC) and calibration using previously derived model coefficients and recalibrated the model using an intercept correction factor that accounted for differences in baseline prevalence of AIN between development and validation cohorts. Results: We included 1982 participants: 1454 at JHH and 528 at Yale. JHH (5%) and Yale (17%) had lower proportions of biopsies with AIN than the development set (23%). The AUC was 0.73 (0.66-0.79) at JHH and 0.73 (0.67-0.78) at Yale, similar to the development set (0.73 (0.64-0.81)). Calibration was imperfect in validation cohorts, particularly at JHH, but improved with application of an intercept correction factor. The model increased AUC of clinicians' prebiopsy suspicion for AIN by 0.10 to 0.77 (0.71-0.82). Conclusions: An AIN diagnostic model retained discrimination in two validation cohorts but needed recalibration to account for local AIN prevalence. The model improved clinicians’ ability to predict AIN.
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