TY - JOUR
T1 - De novo membranous nephropathy (MN) in kidney allografts. A peculiar form of alloimmune disease?
AU - Ponticelli, Claudio
AU - Glassock, Richard J.
PY - 2012/12
Y1 - 2012/12
N2 - De novo membranous nephropathy (MN) is an uncommon complication of kidney transplantation, which shows histological findings similar to those seen in recurrent MN, but with some distinct differences. The clinical presentation may be variable, from asymptomatic to nephrotic proteinuria. The disease may run an indolent course or may have an accelerated course leading to allograft loss. De novo membranous nephropathy (MN) can develop in transplant recipients with viral hepatitis, Alport syndrome, ureteral obstruction, renal infarction, or in conjunction with recurrent IgA nephritis. Histologic signs of allograft rejection are often associated with or can antedate de novo MN. These findings suggest that donor-specific antibodies and antibody-mediated rejection might play a pathogenetic role in some patients with de novo MN. However, signs of rejection were absent in a number of cases, and in some instances the disease developed in recipients of "full house" HLA- matched kidneys. Thus, it seems possible that de novo MN is not because of allograft rejection per se, but is triggered by different injuries that can create an inflammatory environment, activate innate immunity, and expose hidden (cryptic) antigens, probably different from those observed to be involved in idiopathic MN. These events can lead to the production of circulating antibodies and in situ formation of immune complexes (IC) and the morphological lesion of MN.
AB - De novo membranous nephropathy (MN) is an uncommon complication of kidney transplantation, which shows histological findings similar to those seen in recurrent MN, but with some distinct differences. The clinical presentation may be variable, from asymptomatic to nephrotic proteinuria. The disease may run an indolent course or may have an accelerated course leading to allograft loss. De novo membranous nephropathy (MN) can develop in transplant recipients with viral hepatitis, Alport syndrome, ureteral obstruction, renal infarction, or in conjunction with recurrent IgA nephritis. Histologic signs of allograft rejection are often associated with or can antedate de novo MN. These findings suggest that donor-specific antibodies and antibody-mediated rejection might play a pathogenetic role in some patients with de novo MN. However, signs of rejection were absent in a number of cases, and in some instances the disease developed in recipients of "full house" HLA- matched kidneys. Thus, it seems possible that de novo MN is not because of allograft rejection per se, but is triggered by different injuries that can create an inflammatory environment, activate innate immunity, and expose hidden (cryptic) antigens, probably different from those observed to be involved in idiopathic MN. These events can lead to the production of circulating antibodies and in situ formation of immune complexes (IC) and the morphological lesion of MN.
KW - chronic rejection
KW - glomerulonephritis pathogenesis
KW - kidney allograft
KW - membranous nephropathy
KW - proteinuria
KW - transplant glomerulonephritis
UR - http://www.scopus.com/inward/record.url?scp=84869085982&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84869085982&partnerID=8YFLogxK
U2 - 10.1111/j.1432-2277.2012.01548.x
DO - 10.1111/j.1432-2277.2012.01548.x
M3 - Article
C2 - 22909324
AN - SCOPUS:84869085982
VL - 25
SP - 1205
EP - 1210
JO - Transplant International
JF - Transplant International
SN - 0934-0874
IS - 12
ER -