Pathology of Chronic Humoral Rejection. Export

@article{citeulike:3558329, abstract = {Since its initial description in 2001, chronic humoral rejection (CHR, aka 'chronic anti-body-mediated rejection') has been recognized as a distinct and common cause of late graft dysfunction and loss. The pathology is focused on the microvascular components of the kid-ney, manifested by endothelial 'activation', multilamination of glomerular and peritubular capillary basement membranes, interstitial fibrosis and tubular atrophy, and sometimes chronic transplant arteriopathy. Diagnosis requires a biopsy and demonstration of the complement degradation product, C4d in peritubular and/or glomerular capillaries. For definitive diagnosis, detection of donor-specific anti-endothelial antibodies is required (most commonly to class II MHC antigens). Here we review the diagnostic criteria, pathologic manifestations, new molecular markers and related studies in experimental animals.}, author = {Colvin, Robert B B.}, citeulike-article-id = {3558329}, citeulike-linkout-0 = {http://dx.doi.org/10.1159/000170814}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19001815}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19001815}, doi = {10.1159/000170814}, issn = {0302-5144}, journal = {Contributions to nephrology}, keywords = {humoral-rejection, transplant}, pages = {75--86}, posted-at = {2008-11-17 13:12:04}, priority = {2}, title = {Pathology of Chronic Humoral Rejection.}, url = {http://dx.doi.org/10.1159/000170814}, volume = {162}, year = {2009} }

TY - JOUR ID - citeulike:3558329 L3 - citeulike-article-id:3558329 N2 - Since its initial description in 2001, chronic humoral rejection (CHR, aka 'chronic anti-body-mediated rejection') has been recognized as a distinct and common cause of late graft dysfunction and loss. The pathology is focused on the microvascular components of the kid-ney, manifested by endothelial 'activation', multilamination of glomerular and peritubular capillary basement membranes, interstitial fibrosis and tubular atrophy, and sometimes chronic transplant arteriopathy. Diagnosis requires a biopsy and demonstration of the complement degradation product, C4d in peritubular and/or glomerular capillaries. For definitive diagnosis, detection of donor-specific anti-endothelial antibodies is required (most commonly to class II MHC antigens). Here we review the diagnostic criteria, pathologic manifestations, new molecular markers and related studies in experimental animals. JF - Contributions to nephrology SN - 0302-5144 EP - 86 TI - Pathology of Chronic Humoral Rejection. VL - 162 SP - 75 KW - humoral-rejection KW - transplant AU - Colvin, Robert B PY - 2009/// UR - http://dx.doi.org/10.1159/000170814 ER -