Authors:
E. Kamburova (Utrecht, NL)
B. Wisse (Utrecht, NL)
I. Joosten (Nijmegen, NL)
W. Allebes (Nijmegen, NL)
A. Meer (Nijmegen, NL)
L. Hilbrands (Nijmegen, NL)
M. Baas (Nijmegen, NL)
E. Spierings (Utrecht, NL)
E. Hack (Utrecht, NL)
F. Reekum (Utrecht, NL)
A. Zuilen (Utrecht, NL)
M. Verhaar (Utrecht, NL)
M. Bots (Utrecht, NL)
A. Drop (Utrecht, NL)
L. Plaisier (Utrecht, NL)
M. Seelen (Groningen, NL)
J. Sanders (NL)
B. Hepkema (Groningen, NL)
A. Lambeck (Groningen, NL)
L. Bungener (Groningen, NL)
C. Roozendaal (Groningen, NL)
M. Tilanus (Maastricht, NL)
C. Voorter (Maastricht, NL)
L. Wieten (Maastricht, NL)
E. Duijnhoven (Maastricht, NL)
M. Gelens (Maastricht, NL)
M. Christiaans (Maastricht, NL)
F. Ittersum (Amsterdam, NL)
A. Nurmohamed (Amsterdam, NL)
N. Lardy (Amsterdam, NL)
W. Swelsen (Amsterdam, NL)
K. Pant (Amsterdam, NL)
N. Weerd (Amsterdam, NL)
I. Berge (Amsterdam, NL)
F. Bemelman (Amsterdam, NL)
A. Hoitsma (NL)
P. Boog (Leiden, NL)
H. Fijter (Leiden, NL)
M. Betjes (Rotterdam, NL)
S. Heidt (Leiden, NL)
D. Roelen (Leiden, NL)
F. Claas (Leiden, NL)
H. Otten (Utrecht, NL)
In this study all Dutch renal transplant centers and HLA laboratories participated to investigate the impact of pretransplant donor-specific HLA antibodies (DSA), assessed using single antigen bead assays, on long-term graft survival. The clinical significance of these bead assays detection of DSA that do not cause a positive complement-dependent crossmatch is unclear. Currently there is no consensus on how DSA should be included in clinical decision making. As part of the national PROCARE consortium study, all kidney transplantations performed in the Netherlands between 1995-2005, were investigated. From more than 6000 transplantations we were able to collect 4770 pre-transplant sera, 3237 from deceased-donor and 1487 living-donor kidney transplantations, all with a negative complement-dependent crossmatch with current and historic sera. We hypothesized that DSA against HLA class I, II or a combination of both indicate a different risk for kidney graft loss, and compared this between deceased and living-donor transplantations. In living-donor kidney transplantations, we found only a limited and not significant effect on graft survival of pre-transplant DSA against either HLA class I or II antigens. The combined presence of class I and II DSA resulted in a 13% decrease in 10 year death-censored graft survival, from 83% to 70%. In contrast, after deceased donor transplantation, patients with either class I or class II DSA had a 10-year graft survival of 59% and 60% respectively, both significantly lower (p<0.0001) than the 76% graft survival rate of patients without DSA. The combination of DSA against both HLA class I and II antigens resulted in a long-term graft survival of 54% in deceased donor transplantations (p<0.0001). The combined presence of class I and II DSA is a clear risk factor for kidney graft survival both in living and deceased transplantation, whereas for deceased-donor transplantations also HLA class I or class II DSA are indicative for graft failure.