B47-32 Rapidly Progressive Bronchiectasis Following Renal Transplantation: A Rare Association With Mycophenolate Mofetil and Post-transplant Hypogammaglobulinemia

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Abstract Introduction Bronchiectasis is characterized by irreversible airway dilation due to chronic infection, structural airway injury, or an underlying immunologic or genetic disorder. While bronchiectasis can occur in immunocompromised hosts, its development following solid organ transplant is uncommon and typically attributed to recurrent infection or aspiration. Mycophenolate mofetil (MMF) has rarely been associated with pulmonary toxicity and post-transplant hypogammaglobulinemia is an under-recognized contributor to respiratory infection. We present a case of rapidly progressive bronchiectasis in a renal transplant recipient in whom both MMF-related pulmonary toxicity and transplant-associated hypogammaglobulinemia were suspected contributors. Case Description A 74-year-old male with end-stage renal disease status post living-donor kidney transplant (2021) on prednisone, tacrolimus, and MMF presented with progressive productive cough and dyspnea. He had no significant smoking history, no known chronic aspiration, and no childhood respiratory disease. Pre-transplant imaging (2021) demonstrated normal pulmonary airways. Post-transplant imaging (2023) demonstrated multi-lobar cylindrical bronchiectasis with tree-in-bud nodularity. Extensive evaluations for nontuberculous mycobacteria, fungal pathogens, allergic bronchopulmonary aspergillosis, autoimmune disease, and α-1 antitrypsin deficiency were negative. Immunoglobulin testing revealed persistent hypogammaglobulinemia. The patient’s airway findings progressed despite airway clearance therapy, inhaled tobramycin, and repeated antibiotic courses. To address disease progression and subclass deficiency, tacrolimus was discontinued and belatacept was initiated while the MMF dose was decreased. Despite these changes in his immunosuppressive regimen, his bronchiectasis continued to worsen. Given the unusual onset and rapid progression, multidisciplinary review raised concern for MMF-related bronchial injury versus bronchiectasis secondary to immune dysregulation from hypogammaglobulinemia. Immunosuppression adjustments and IVIG therapy were initiated. Transbronchial lung biopsy demonstrated acute inflammatory infiltrate with culture and pathology-confirmed Stenotrophomonas maltophilia, a rare tissue-level confirmation of this organism, which is often presumed to be a colonizer rather than a true pathogen. This supported its role in ongoing airway injury and structural progression. Infectious disease submitted biopsy isolates for minocycline susceptibility testing to assess the potential for chronic suppressive therapy. Discussion This case highlights uncommon contributors to bronchiectasis in transplant recipients. MMF has been implicated in isolated reports of pulmonary toxicity, though a causal relationship to bronchiectasis remains poorly defined. Hypogammaglobulinemia may predispose to progressive bronchiectatic change and recurrent infection. Biopsy-proven Stenotrophomonas emphasizes that this organism should not be routinely dismissed as a colonizer in immunocompromised patients. Distinguishing between drug-related pulmonary injury and immune-mediated susceptibility is essential, as management differs substantially. Early recognition, immunosuppression adjustment, IVIG when indicated, and susceptibility-guided antimicrobial therapy may help mitigate progression and reduce infectious complications. This abstract is funded by: None

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