PMID- 25054778
OWN - NLM
STAT- MEDLINE
DCOM- 20160425
LR  - 20211021
IS  - 1523-1755 (Electronic)
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 87
IP  - 2
DP  - 2015 Feb
TI  - A closer look at rituximab induction on HLA antibody rebound following 
      HLA-incompatible kidney transplantation.
PG  - 409-16
LID - 10.1038/ki.2014.261 [doi]
AB  - Rituximab has been used to increase the efficacy of desensitization protocols for 
      human leukocyte antigen (HLA)-incompatible kidney transplantation; however, 
      controlled comparisons have not been reported. Here we examined 256 
      post-transplant HLA antibody levels in 25 recipients desensitized with and 25 
      without rituximab induction, to determine the impact of B-cell depletion. We 
      found significantly less HLA antibody rebound in the rituximab-treated patients 
      (7% of donor-specific antibodies (DSAs) and 33% of non-DSAs) compared with a 
      control cohort desensitized and transplanted without rituximab (32% DSAs and 55% 
      non-DSAs). The magnitude of the increase was significantly larger among patients 
      who did not receive rituximab. Interestingly, in rituximab-treated patients, of 
      the 39 HLA antibodies that increased post transplant, 34 were specific for HLA 
      mismatches present in previous allografts or pregnancies, implying limited 
      efficacy in memory B-cell depletion. Compared with controls, rituximab-treated 
      patients had a significantly greater mean reduction in DSA (-2505 vs. -292 mean 
      fluorescence intensity), but a similar rate of DSA persistence (52% in rituximab 
      treated-and 40% in non-treated recipients). Thus, rituximab induction in 
      HLA-incompatible recipients reduced the incidence and magnitude of HLA antibody 
      rebound, but did not affect DSA elimination, antibody-mediated rejection, or 
      5-year allograft survival when compared with recipients desensitized and 
      transplanted without rituximab.
FAU - Jackson, Annette M
AU  - Jackson AM
AD  - Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.
FAU - Kraus, Edward S
AU  - Kraus ES
AD  - Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.
FAU - Orandi, Babak J
AU  - Orandi BJ
AD  - Department of Surgery, Johns Hopkins University, Baltimore, Maryland, USA.
FAU - Segev, Dorry L
AU  - Segev DL
AD  - Department of Surgery, Johns Hopkins University, Baltimore, Maryland, USA.
FAU - Montgomery, Robert A
AU  - Montgomery RA
AD  - Department of Surgery, Johns Hopkins University, Baltimore, Maryland, USA.
FAU - Zachary, Andrea A
AU  - Zachary AA
AD  - Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.
LA  - eng
GR  - R01 DK098431/DK/NIDDK NIH HHS/United States
GR  - RC1 DK086731/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20140723
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (HLA Antigens)
RN  - 0 (Isoantibodies)
RN  - 4F4X42SYQ6 (Rituximab)
SB  - IM
CIN - Kidney Int. 2015 Feb;87(2):277-9. PMID: 25635721
MH  - Adult
MH  - B-Lymphocytes/immunology
MH  - Desensitization, Immunologic
MH  - Female
MH  - *HLA Antigens
MH  - Histocompatibility Testing
MH  - Humans
MH  - Immunologic Memory
MH  - Isoantibodies/*biosynthesis
MH  - *Kidney Transplantation
MH  - Lymphocyte Activation
MH  - Lymphocyte Depletion
MH  - Male
MH  - Middle Aged
MH  - Rituximab/*therapeutic use
MH  - Time Factors
PMC - PMC4305036
MID - NIHMS608433
EDAT- 2014/07/24 06:00
MHDA- 2016/04/26 06:00
PMCR- 2015/08/01
CRDT- 2014/07/24 06:00
PHST- 2014/03/24 00:00 [received]
PHST- 2014/05/22 00:00 [revised]
PHST- 2014/06/05 00:00 [accepted]
PHST- 2014/07/24 06:00 [entrez]
PHST- 2014/07/24 06:00 [pubmed]
PHST- 2016/04/26 06:00 [medline]
PHST- 2015/08/01 00:00 [pmc-release]
AID - S0085-2538(15)30050-8 [pii]
AID - 10.1038/ki.2014.261 [doi]
PST - ppublish
SO  - Kidney Int. 2015 Feb;87(2):409-16. doi: 10.1038/ki.2014.261. Epub 2014 Jul 23.