Comparison of group 1 and 2:
BKV viremia rate was found to be 3.5% (nephropathy rate 1%). There was no difference between the groups in terms of gender, CKD etiology, donor age, viral hepatitis, mismatch numbers (p: 0.980), rate of MPA and EVE use (Table 1). Among the clinical outcomes, the need for postoperative hemodialysis (HD), chronic allograft dysfunction (CAD), development of new-onset diabetes mellitus after transplantation, malignancy development rates, patient and graft loss rates, patient survival rates and serum Cr and GFR mean value at the last control were found to be similar (Table 2). In the 2nd group, it was determined that 34 (26.4%) of 129 patients developed BKPyVAN, 19 (14.7%) had graft loss and 7 (5.5%) of them were due to BKPyVAN.
Recipient age, body mass index, cadaveric transplant rate, anti-thymocyte globulin (ATG) use rate in induction therapy, TAC / MPA / prednisolone use rate (n = 120, 93%), the rates of AR (humoral/cellular), delayed graft function (DGF), cytomegalovirus (CMV) viremia and vesicoureteral reflux rates to transplant kidney were higher in group 2. Graft survival rates were shown to be lower in the BKV group (group 1 and 2, respectively, 1st-3rd-5th-10th year; 95.4% / 96.9- 92.8 / 89.8- 90.4 / 78.7- 85.7 / 65, p: 0.01). While TAC was used more, CSA and sirolimus (SRL) less in the second group, MPA and EVE were used with similar rates. It was shown that in all patients who used low-dose CNI + m-TORi (n=8, 6,2%), the viremia / BKPyVAN ratio was lower and the ratio was significantly higher in the TAC + MPA protocol (Table 1).
In logistic regression analysis, the presence of AR, elderly recipient, cadaveric transplantation, ATG and TAC use and, CMV viremia were shown to be predictive factors for BKV development (Table 3).
Patients who had AR before ISP change (AR +/-, n = 33/96, respectively) had lower graft survival rates (1st-3rd-5th-10th year, respectively, AR (+): %93/84/72/43, AR (-): 97/93/84/77, p: 0.045), and graft functions (Cr values higher in all three measurements, lower GFR levels, p: <0.001) were shown to be worse.
Group 2a (swiching to low dose TAC plus EVE, n=54) / Group 2b (swiching to others ISP, n=75) comparisons;
It was found that there was no difference between the groups in terms of demographic and immunological parameters. However, CKD etiologies, cadaveric transplant rates, mismatch numbers, RRT modalities, induction therapies, TAC and ATG usage rates, CAD, DGF, CMV rates, graft / patient survival rates were similar for the two groups. BKPyVAN ratio was higher in group 2a (Group 2a/ 2b, respectively 23 (42.6%)/ 11 (14.7%), p: <0.001). Graft losses were found in 9 patients in group 2a (in 5 (55.5%) patients were due to BKPyVAN) and 10 patients in group 2b (in 2 patients (20%) were due to BKPyVAN) (p: 0.507). It was observed that BKV DNA levels showed a fluctuating course: higher in group 2b at the first measurements, similar between the groups in the following measurements, and higher in group 2a at the last measurement (Figure 1).
In terms of graft functions, the 1st and 3rd measurements were similar, while the second measurements showed worse graft functions in the group 2a. In summary, it was found that graft functions were impaired after changing the protocol in group 2a, but there was no difference between the last controls (long term).
The graft loss rates (Group 2a-2b, respectively, 9 (16.7%) - 10 (13.3%), p: 0.598) and biopsy findings (glomerulitis, interstitial inflammation, tubulitis, chronic glomerulopathy, interstitial fibrosis, tubular atrophy, SV40 (+), C4d (+), transplant glomerulopathy) were found to be similar between the groups. The rate of using cidofovir was higher in group 2a (Group 2a/ 2b, respectively 18.5%/ 5.3%, p: 0.018). Before the ISP change, the AR rates were found to be high in the EVE arm for both 129 patients (Group 2a/2b; 38.9%/ 16%, p: 0.003) and the patients with PCR ≥104 (Group 2a/2b; 36.7%/ 7.4%, p: 0.005, respectively). After the ISP change, the AR rates were similar (Group A-B 13% / 5.3%, p: 0.2, respectively).
Comparisons of those with viral load ≥104- <104:
In the analyzes carried out independently from the ISP, while the graft survival rates were lower in those with ≥104 than those with <104 (respectively 1st-3rd-5th-10th year ≥104/ <104; 94/ 98- 88/ 96- 73/ 91- 41/ 85, p: 0.017), the graft functions were shown to be similar between the groups in all three measurements. It was found that BKPyVAN did not develop in patients with BKV DNA <104, whereas it developed in 34 (44.7%) patients (p: <0.001) in those with ≥104. It was determined that 15 of the graft losses were developed in patients with viral load ≥104; 4 were the patients with viral load <104 (rejection in 2 patients, CAD in 1 patient, patient loss in 1 patient). There was no significant difference between rates of graft loss due to BKPyVAN (≥104/ <104; 7 (46.7%) / 0, p: 0.245, respectively).
In the subgroup analyses of 76 patients with only BKV PCR ≥104 (Group 2a/ 2b: 49/27); demographic data, graft / patient survival rates, graft function, and other clinical outcomes were similar between the groups. The negative, decreased to <104 and remained ≥104 rates of BKV DNA levels after ISP change were similar in group 2a/2b (group 2a (36.7- 30.6-32.7%, respectively) / 2b (40.7- 29)). , 6- 29.6%), p: 0.937). Acute rejection rates were higher in Group 2a before the ISP change (Group 2a/ 2b 36.7% / 7.4%, p: 0.005), and (Group 2a/ 2b, respectively 12.2% / 3.7%). p: 0.410) were found to be similar after ISP change.
Fifty-three patients with BKV PCR <104 only (Group 2a/ 2b: 5/48); were divided into subgroups as the patients without ISP change (n = 21) and those with all ISP change (n = 32). Demographic data, mean PCR levels, graft survival rates, graft functions, rejection rates and all other clinical outcome rates were shown to be similar between the groups.