Posttransplant Tubulointerstitial Nephritis in Kidney Recipients: From Bacteria to BK Virus: A 24-Year Single-Center Analysis of Etiology, Timing, and Graft Survival.

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.