Acute Interstitial Nephritis (AIN) Following Bee Stings: A Rare Etiology of Progressive Kidney Failure

Introduction: AIN remains an overlooked cause of kidney disease, often masked by nonspecific clinical features and a broad differential. While drug hypersensitivity reactions and autoimmune processes are well-known culprits, environmental triggers are seldom implicated. We report a rare case of AIN in a patient after multiple bee stings—highlighting the importance of considering unusual etiologies in progressive kidney dysfunction. Case Description: A 39-year-old male presented with fatigue, anuria, and a serum creatinine of 19.7 mg/dL. Medical history was unremarkable, except for hundreds of bee stings one month prior. Renal biopsy revealed patchy interstitial inflammation with mononuclear cells and eosinophils, along with chronic changes including interstitial fibrosis, tubular atrophy, and glomerulosclerosis. Immunohistochemistry showed CD3+ T-lymphocytes and CD20+ B-cells, with negative IgG4 staining. Histological examination and clinical timeline confirmed AIN likely secondary to a hypersensitivity reaction to bee venom. Despite corticosteroid therapy, renal function deteriorated, necessitating long-term dialysis. Discussion: Bee venom, rich in melittin and phospholipase A2, induces tubular injury and immune responses. The pathogenesis of bee venom–induced nephritis may involve both direct cytotoxicity and delayed-type hypersensitivity [1,2]. Biopsy findings, with no drug exposure or infection, suggest an immune-mediated response. Results raise a CKD dilemma: is inflammation a cause or a response to chronic injury? However, the distribution and activity of inflammation suggest a primary injurious process. While such cases are rare, prior reports have documented similar findings after envenomation [1–5]. Clinicians should be aware of this link, particularly when common etiologies are ruled out.