Abemaciclib-associated acute interstitial nephritis successfully treated with glucocorticoids: a case report and literature review.

Background: Drug-induced acute interstitial nephritis (DI-AIN) is the most common type of AIN. DI-AIN occurs when medications trigger a T cell-mediated immune response that promotes tubulitis and interstitial inflammation with eosinophils, often resulting in acute kidney injury (AKI) with nephromegaly. Recently, prolonged use of cyclin-dependent kinase (CDK) 4/6 inhibitors, as oral molecular-targeted drugs for breast cancer, was identified as a cause of AKI, including AIN and acute tubular necrosis (ATN). To date, there have been no reported cases of AIN associated with the use of abemaciclib, a CDK4/6 inhibitor.

Case presentation: A 66-year-old Japanese woman presented with persistent diarrhea and nausea shortly after the initiation of abemaciclib for breast cancer and was subsequently referred to our hospital with severe renal dysfunction (blood urea nitrogen, 128.7 mg/dL; creatinine, 15.16 mg/dL). Based on her elevated renal tubular damage markers and bilateral renal enlargement, acute renal failure was suspected. A renal biopsy revealed interstitial infiltration of mononuclear cells and eosinophils, along with tubulitis and epithelial cell damage within the renal tubules, suggesting AIN caused by abemaciclib. The renal function improved with glucocorticoid therapy following fluid replacement for pre-renal AKI, and the serum creatinine decreased to approximately 2 mg/dL within 2 months.

Conclusions: We report a case of biopsy-proven AIN that developed shortly after the initiation of abemaciclib, leading to severe renal dysfunction with nephromegaly. While prolonged use of CDK4/6 inhibitors can cause both AIN and ATN, AIN can also occur after short-term use, highlighting the importance of a renal biopsy to determine the need for glucocorticoid therapy.

Clinical trial number: Not applicable.