Therefore, it may perform differently in patient and disease subsets. For example, Maluf et al.[19] found that the same DRI score predicts significantly worse outcomes for HCV-positive

patients than in HCV-negative recipients. For these reasons, we developed a donor risk model specific to HCV-positive recipients in the MELD era of LT, and focused on AA recipients because check details of their previously described poor long-term graft survival. There is currently a donor shortage in Western countries. In 2009, the United States alone had 26% of patients listed for liver transplant die or become too ill to transplant.[17] Most patients removed from the list without transplant receive at least one offer before they dropped off the list and most of those offers are refused for perceived issues of donor quality.[20] The ability to utilize older donors in specific patient subsets without compromising outcomes provides a modest means of expanding the donor pool and potentially reducing wait-list mortality. The matching of AA donors with HCV-positive AAs has previously been criticized as too impractical selleck kinase inhibitor to apply to day-to-day donor selection.[21] However, given the significant risk of graft loss within 5 years for AA with non-AA donors, especially older non-AA donors, plausible clinical scenarios that may allow matching of AA donors

to AA recipients should be considered. The AADRI-C may also be useful in identifying AA recipients at highest risk for graft loss Branched chain aminotransferase who may benefit from more intensive monitoring and/or early HCV treatment post-LT. An HCV-positive AA recipient transplanted with a high AADRI-C graft (>2.44) has a predicted 3-year graft survival of only 53% compared to 3-year

survival with a low AADRI-C (<1.6) donor of 77%. A clinician might target this high AADRI-C recipient for timely antiviral therapy. The underlying pathogenesis linking AA-derived allografts with improved postliver transplant outcomes in AAs is unclear. In a pretransplant setting, AAs carry a disproportionate burden of HCV infection in the U.S. population and there is epidemiological evidence suggesting AAs spontaneously clear acute HCV infection less often than non-AAs.[22-24] However, chronically infected AAs may actually progress to cirrhosis more slowly than Caucasians.[25] Investigators have looked for racial differences in immune response to HCV that explain the apparent dichotomy in AA outcomes with HCV infection acutely and chronically. It has been theorized that ethnic trends in HLA typing and KIR type predicts spontaneous viral clearance and sustained virological response to interferon-based therapy.[26] For example, HLA-A*02 and HLA-DRB1*12 genotypes were associated with treatment-induced viral clearance in non-Caucasians but not in Caucasians, and natural killer cell immunoglobulin receptor KIR2DL3 was associated with both treatment and spontaneous clearance in HLA-C patients.