TY  - JOUR
AU  - Dragun, D
AU  - Muller, DN
AU  - Brasen, JH
AU  - Fritsche, L
AU  - Nieminen-Kelha, M
AU  - Dechend, R
AU  - Kintscher, U
AU  - Rudolph, B
AU  - Hoebeke, J
AU  - Eckert, D
AU  - Mazák, István
AU  - Plehm, R
AU  - Schonemann, C
AU  - Unger, T
AU  - Budde, K
AU  - Neumayer, HH
AU  - Luft, FC
AU  - Wallukat, G
TI  - Angiotensin II type 1-receptor activating antibodies in renal-allograft rejection
JF  - NEW ENGLAND JOURNAL OF MEDICINE
J2  - NEW ENGL J MED
VL  - 352
PY  - 2005
IS  - 6
SP  - 558
EP  - 569
PG  - 12
SN  - 0028-4793
DO  - 10.1056/NEJMoa035717
UR  - https://m2.mtmt.hu/api/publication/1844642
ID  - 1844642
AB  - BACKGROUND Antibodies against HLA antigens cause refractory allograft rejection with vasculopathy in some, but not all, patients. METHODS We studied 33 kidney-transplant recipients who had refractory vascular rejection. Thirteen had donor-specific anti-HLA antibodies, whereas 20 did not. Malignant hypertension was present in 16 of the patients without anti- HLA antibodies, 4 of whom had seizures. The remaining 17 patients had no malignant hypertension. We hypothesized that activating antibodies targeting the angiotensin II type 1 (AT(1)) receptor might be involved. RESULTS Activating IgG antibodies targeting the AT(1) receptor were detected in serum from all 16 patients with malignant hypertension and without anti- HLA antibodies, but in no other patients. These receptor-activating antibodies are subclass IgG1 and IgG3 antibodies that bind to two different epitopes on the second extracellular loop of the AT(1) receptor. Tissue factor expression was increased in renal-biopsy specimens from patients with these antibodies. In vitro stimulation of vascular cells with an AT(1)-receptor-activating antibody induced phosphorylation of ERK 1/2 kinase and increased the DNA binding activity of the transcription factors activator protein 1 (AP-1) and nuclear factor-kappaB. The AT(1) antagonist losartan blocked agonistic AT(1) - receptor antibody - mediated effects, and passive antibody transfer induced vasculopathy and hypertension in a rat kidney-transplantation model. CONCLUSIONS A non-HLA, AT(1) - receptor - mediated pathway may contribute to refractory vascular rejection, and affected patients might benefit from removal of AT(1) - receptor antibodies or from pharmacologic blockade of AT(1) receptors.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Opelz, Gerhard
ED  - =Collaborative, Transplant Study / Collaborative Organization
ED  - Szenohradszky, Pál / Collaborator
ED  - Szederkényi, Edit / Collaborator
ED  - Marofka, Ferenc / Collaborator
TI  - Non-HLA transplantation immunity revealed by lymphocytotoxic antibodies
JF  - LANCET
J2  - LANCET
VL  - 365
PY  - 2005
IS  - 9470
SP  - 1570
EP  - 1576
PG  - 7
SN  - 0140-6736
DO  - 10.1016/s0140-6736(05)66458-6
UR  - https://m2.mtmt.hu/api/publication/31285571
ID  - 31285571
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Iványi, Béla
AU  - Haszon, I
AU  - Börcsökné Endreffy, Emőke
AU  - Szenohradszky, Pál
AU  - Petri, I B
AU  - Kalmár, Tibor
AU  - Butkowski, R J
AU  - Charonis, A S
AU  - Túri, Sándor
TI  - Childhood membranous nephropathy, circulating antibodies to the 58-kD TIN antigen, and anti-tubular basement membrane nephritis: An 11-year follow-up
JF  - AMERICAN JOURNAL OF KIDNEY DISEASES
J2  - AM J KIDNEY DIS
VL  - 32
PY  - 1998
IS  - 6
SP  - 1068
EP  - 1074
PG  - 7
SN  - 0272-6386
DO  - 10.1016/S0272-6386(98)70085-X
UR  - https://m2.mtmt.hu/api/publication/1029117
ID  - 1029117
LA  - English
DB  - MTMT
ER  -