BK Virus-Associated Immune-Mediated Tubulointerstitial Nephritis. Clinicopathologic Characterization.
Jing Xu, Abdel Abdullatif, Graham Towns, Lillian Gaber, Roberto Barrios, Luan Truong. Changhai Hospital, Shanghai, China; Methodist Hospital, Houston, TX
Background: BK virus-associated immune-mediated tubulointerstitial nephritis (BKV TIN) is a form of chronic tubulointerstitial nephritis chacterized by tubular basemen membrane (TBM) deposition of immunoglulins and complement components, against the background of BKV nephropathy. TBM immune-type electron dense deposits are also noted in several cases. The knowledge on BKV TIN is limited.
Design: All renal transplant biopsies during a 10-year period ( 2000-2010) were reviewed to identify those with BKV nephropathy alone and those with BKV-TIN. Their clinicopathologic features were compared and contrasted.
Results: Among 730 renal tranplant (Tx) biopsies, 13 biopsies in 9 patients showed BKV+TIN (Group A), and 29 biopsies in 25 patients showed BKV nephropathy only (Group B). TIN with TBM deposition of immunoglobulin G (Ig G) and complement com ponent C3 (C3) was noted in one Tx biopsy without BKV nephropathy. The age and sex in Groups A and B patients were similar (60.3±11.6 vs 60.7±10.6 years; F/M ratio 0.7 vs 0.6 ). There was no significant difference in the serum creatinine at presentation (2.7±1.8 vs 2.9±1.2mg/dl), the baseline immunosupression, or the blood BKV level by PCR between the two groups. TBM IgG, C3 and C4d for Groups A and B was 100% vs 0%, rare-20% of tubular profiles; 100% vs 31%, few -25% of tubular profiles; and 92 vs 24%, few-30% tubular profiles. TBM electron dense deposits were noted in 2 cases on routine EM. TBM did not show the large T antigen by immunostain in any case of Groups A or B. Chronic tubulointetstitial injury was more severe in Group A (34.0±29.5% vs 27.7±21.4 % of cortical tissue). Multiple biopsies done in four patients in Group A showed that BKV TIN was preceded by BKV nephropathy alone (3 cases), persisted in repeated biopsies (2 cases), or disappeared in repeated biopsy in which BKV nephropathy persisted (1 case).
Conclusions: BKV TIN is probably pathogenetically related to BKV nephropathy since it develops rather frequently (30%) from the background of BKV nephropathy, but only rarely observed in renal Tx biopsy without BKV nephropathy. It seems to be associated with more renal chronic renal injury compared with BKN nephropathy alone. Its evolution is variable with possible persistence of resolution in repeated biopsies.
Wednesday, March 2, 2011 9:30 AM
Poster Session V # 232, Wednesday Morning