PMID- 21030904
OWN - NLM
STAT- MEDLINE
DCOM- 20110128
LR  - 20220408
IS  - 1534-6080 (Electronic)
IS  - 0041-1337 (Linking)
VI  - 90
IP  - 12
DP  - 2010 Dec 27
TI  - Anti-angiotensin type 1 receptor antibodies associated with antibody mediated 
      rejection in donor HLA antibody negative patients.
PG  - 1473-7
LID - 10.1097/TP.0b013e3181fd97f1 [doi]
AB  - BACKGROUND: Angiotensin type 1 receptor (AT1R) mediates most physiologic and 
      pathophysiologic actions of its endogenous ligand, angiotensin II, with 
      overactivity leading to vascular remodeling and hypertension. Antibodies to AT1R 
      are implicated in several vascular pathologies. The aim of our study was to 
      determine the impact of antibody to AT1R on clinical outcomes including antibody 
      mediated rejection (AMR), with or without C4d deposition, in patients whose sera 
      contained no donor human leukocyte antigen (HLA)-specific antibody (HLA-DSA). 
      METHODS: Pretransplant sera from 97 recipients and sera obtained at the time of 
      acute rejection (AR) were tested by Luminex-based single-antigen bead assays to 
      determine HLA-DSA and antibodies to major histocompatibility class I 
      chain-related gene A (MICA). The presence of antibody to AT1R was determined by a 
      cell-based ELISA method using a cutoff of 17 units to distinguish high from low 
      binding. RESULTS: Sera from 63 recipients were determined to have no HLA-DSA and 
      no donor-specific MICA antibodies pretransplant and at the time of AR, and 16 of 
      these recipients were diagnosed with AR including 7 with AMR and 9 with cellular 
      AR (cell-mediated rejection). High-binding AT1R antibodies were identified for 
      six of seven in the AMR+ group and zero of nine in the cell-mediated rejection+ 
      group (P=0.0009). CONCLUSIONS: A strong association was observed between the 
      presence of high binding to AT1R and AMR in recipients whose sera contained no 
      antibody to donor HLA or MICA. Assessing the AT1R antibody status along with the 
      HLA-DSA provides additional information to determine the immunologic risk for 
      recipients.
FAU - Reinsmoen, Nancy L
AU  - Reinsmoen NL
AD  - Cedars-Sinai Medical Center, HLA Laboratory, Comprehensive Transplant Center, Los 
      Angeles, CA 90048, USA. nancy.reinsmoen@cshs.org
FAU - Lai, Chih-Hung
AU  - Lai CH
FAU - Heidecke, Harald
AU  - Heidecke H
FAU - Haas, Mark
AU  - Haas M
FAU - Cao, Kai
AU  - Cao K
FAU - Ong, Geraldine
AU  - Ong G
FAU - Naim, Mehrnoush
AU  - Naim M
FAU - Wang, Qi
AU  - Wang Q
FAU - Mirocha, James
AU  - Mirocha J
FAU - Kahwaji, Joseph
AU  - Kahwaji J
FAU - Vo, Ashley A
AU  - Vo AA
FAU - Jordan, Stanley C
AU  - Jordan SC
FAU - Dragun, Duska
AU  - Dragun D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Transplantation
JT  - Transplantation
JID - 0132144
RN  - 0 (Antibodies)
RN  - 0 (Autoantibodies)
RN  - 0 (HLA Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Receptor, Angiotensin, Type 1)
SB  - IM
MH  - Acute Disease
MH  - Antibodies/*blood/immunology
MH  - Antibody Specificity
MH  - Autoantibodies/immunology
MH  - Chromosomes, Human, Pair 3
MH  - Chronic Disease
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Graft Rejection/*immunology
MH  - HLA Antigens/*immunology
MH  - Histocompatibility Antigens Class I/genetics
MH  - Humans
MH  - Immunity, Cellular
MH  - Kidney Failure, Chronic/etiology/surgery
MH  - Kidney Transplantation/*immunology
MH  - Receptor, Angiotensin, Type 1/genetics/*immunology
MH  - *Tissue Donors
EDAT- 2010/10/30 06:00
MHDA- 2011/02/01 06:00
CRDT- 2010/10/30 06:00
PHST- 2010/10/30 06:00 [entrez]
PHST- 2010/10/30 06:00 [pubmed]
PHST- 2011/02/01 06:00 [medline]
AID - 10.1097/TP.0b013e3181fd97f1 [doi]
PST - ppublish
SO  - Transplantation. 2010 Dec 27;90(12):1473-7. doi: 10.1097/TP.0b013e3181fd97f1.