*Purpose: Transplantation of hepatitis C viremic (HCV) donor kidneys into uninfected recipients (D+/R-) is becoming more common in the United States. However, the long-term risks associated with HCV viremic) donor transplants are still unknown. Recent ‘transmit-and-treat’ studies have suggested that donor HCV might be associated with an increased risk of BK polyomavirus (BKPyV) and CMV infections. It has been suggested that this may be due to the suppression of host immune response due to HCV. We have previously reported a HCV transmission rate of only 9% with an ultra-short pangenotypic DAA prophylaxis of 2- 7days. Here we report the incidence of BKPyV and cytomegalovirus (CMV) infections in this cohort and compare these rates with a matched cohort (1:1 fashion) of HCV D-/R- KTR.

*Methods: All patients received induction with rabbit anti-thymocyte globulin followed by triple immunosuppression with tacrolimus, mycophenolate and prednisone. D-/R- KTR in our center (controls) were matched with cases (D+/R-) in a 1:1 distribution based upon the following: a) transplant time period in the post-kidney allocation system (KAS) era (January 2015 onwards), b) ‘kidney-only’ transplant with ≤1 previous organ transplant, c) pre-transplant diabetes, d) EPTS score category measured in quintiles (0-20%, 21-40%, 41-60%, 61-80%, 81-100%) d) cPRA at transplant <50%; e) negative crossmatch at transplant; and f) DSA at transplant≤3000 MFI.

*Results: A total of 102 D+/R- transplants (mean age=52) were included with the following distribution; Group 1 (2-4d prophylaxis; N=52) and Group 2 (7d prophylaxis; N=50). Of the 9 patients that developed viremia, all patients achieved sustained virologic response post-full course therapy. Controls (N=102; D-/R-) were more likely to be African-American (73% vs 59%; p=0.04), have pre-formed donor specific antibodies at transplant (13% vs 3%, p=0.02) and have higher KDPI (mean 66 vs 56, p=0.001) compared with D+/R- recipients. The two groups were well-matched with other aforementioned matching criteria including CMV donor-recipient seromismatch. Recipients of HCV D+/R- had equivalent CMV infection (14% vs 14%, p=1.0) but less CMV disease compared to controls (71% vs 29%, p=0.05) amongst those who developed viremia. There was a numerically higher incident risk of any BKPyV infection (20% vs 12%, p=0.12), and high plasma titer BKPyV ≥10000 (12% vs 6%, p=0.21) in the D+/R- group compared with D-/R- group that did not reach statistical significance.

*Conclusions: In this large single-center study of HCV NAT+ transplants, we did not find an increased risk of CMV infections. There was a numerical trend for increased BKPyV that was seen predominantly in patients without HCV replication. These data suggest one of two possibilities: One, lack of HCV replication may be protective against CMV; or two, that the apparent increased risk of opportunistic viral infections may be due to unmeasured confounders in patient selection.

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