Merih TEPEOGLU, B. Handan OZDEMIR, Alev Ok ATILGAN, Eda YILMAZ, Mohammadamin Ghaffari SOLEIMANI, Mehmet HABERAL
Experimental and Clinical Transplantation - 2026;24(9):689-698
Objectives: Tubulointerstitial nephritis is a notable cause of graft dysfunction following kidney transplant. We comprehensively evaluated tubulointerstitial nephritis epidemiology, clinical presentation, histopathology, and graft survival outcomes in a single-center cohort over a period of 24 years. Materials and Methods: We conducted a retrospective analysis of 209 biopsy-proven tubulointerstitial nephritis cases among 1445 kidney transplant recipients at Başkent University Ankara Hospital (2000-2024). Etiologies included bacterial, BK virus-associated nephropathy, granulomatous inflammation, cytomegalovirus, and adenovirus. Clinical symptoms, timing of onset, rejection overlap, and persistence of inflammation or viremia were analyzed, alongside graft survival metrics. Results: Bacterial tubulointerstitial nephritis was most common (50.7%; prevalence 7.3%), with a median onset beyond 1 year in 72.6% of cases. Cases of BK virus-associated nephropathy comprised 42.6% (6.1% prevalence), with 41.6% of cases presenting after 12 months. Granulomatous tubulointerstitial nephritis constituted 5.3%, whereas cytomegalovirus and adenovirus tubulointerstitial nephritis were rare (1.4%). Symptomatic presentation occurred in 62.3% of bacterial cases and 59.3% overall. Concurrent antibody-mediated rejection and persistent inflammation or viremia significantly reduced 10-year graft survival across etiologies (bacterial was 60% vs 90%, P < .005; BK virus-associated nephropathy was 40% vs 70.7%, P = .005; persistent inflammation was ~20% survival for viral tubulointerstitial nephritis). Postdiagnosis survival for patients with viral tubulointerstitial nephritis averaged 22.9 months, with 0% 10-year survival. Conclusions: Tubulointerstitial nephritis after transplant is a heterogeneous and under recognized cause of graft loss. Etiology-specific profiling, prolonged surveillance (including BK polymerase chain reaction results), early histology evaluation, and individualized immunosuppressive and antimicrobial strategies are essential for outcome optimization.
