COMPLICATIONS - INFECTIONS

H. Dheir¹, S. Sen², A. Zeytinoglu³, M. Yilmaz¹, B. Sarsik², F. Kircelli¹, H. Toz^1
1Nephrology, Ege University Medical School, Izmir/TURKEY, ²Pathology, Ege University Medical School, Izmir/TURKEY, ³Microbiology, Ege University Medical School, Izmir/TURKEY

Body: Introduction Polyoma virus associated nephropathy is an infectious complication of kidney transplantation (Tx). The risk factors and diagnostic procedures are defined. The impact of routine surveillance strategies with viremia and protocol biopsies need to be clarified. Methods During the study period routine screening of BK viremia was adopted at 3, 6, 9 and 12^th months post-Tx. Additionally, as a center policy, protocol biopsies were performed at 6, 12, 36, 60 (and optionally 3) months post-Tx. Quantitative BKV DNA was investigated by a real-time PCR assay (LC PCR, Germany). Protocol biopsies showing tubulointerstitial inflammation and/or tubular regenerative changes, and all the indication biopsies were stained with anti–simian virus 40 (SV40) antibody. Polyoma virus infection was identified using morphology and positivity of immunoperoxidase staining with anti–SV40. Results Study population was consisted of 11 PVAN cases among 218 consecutive adult kidney Tx patients (5 %). Four of them manifested with acute allograft dysfunction at a mean of 6.9±3.6 (3.4-10.7) months post-Tx. Mean serum creatinine and BK viremia were 2.17±0.67 mg/dL and 2091±1920 copies/mL, respectively. One patient had no detectable viremia in spite of positive anti-SV40 staining. Seven of 11 patients were diagnosed as PVAN at the time of routine viremia and protocol biopsy surveillance. Two of 7 patients were diagnosed at 3^rd, remaining at 6^th month post-Tx. Mean serum creatinine and BK viremia were 1.25±0.38 mg/dL and 4800±4178 copies/mL, respectively. One patient had no detectable viremia in spite of positive anti-SV40 staining and the presence of histological changes indicative for viral infection. Reduction of overall immunosuppressive regimen applied to all patients. Additionally, intravenous immunoglobulin (n:5), leflunamid (n:1), conversion to azathioprine or sirolimus (n:3) were the adjunctive treatment approaches. All patients were followed at least a year (mean: 26±11, range: 13-43 months after the diagnosis of PVAN), and no graft loss occurred during this period. After the diagnosis of PVAN, 18 control biopsies were performed in 11 patients with regular intervals (mean number of biopsy per patient: 1.6). AntiSV40 positivity was disappeared in 7 of 11 patients within first 12 months after PVAN. On the other hand, anti-SV40 positivity persisted in 3 patients at 12 month and in 1 patient at 18 months after PVAN. Baseline demographic and clinical features, and presence or absence of allograft dysfunction at the diagnosis of PVAN were not different between two groups. The only remarkable feature was the slightly higher BK viremia at diagnosis in persisted group (7133±4850 copies/mL) than resolved group (2297±1741 copies/mL, p=0.05). Conclusion Routine surveillance with BK viremia and protocol biopsies may allow diagnosing the PVAN before the occurrence of graft dysfunction in more than half of the patients. Outcome is excellent although the persistent nature is observed in some patients.

Disclosure: All authors have declared no conflicts of interest.