The spectrum of antibody-mediated renal allograft injury: Implications for treatment

被引:101
作者
Gloor, J. [1 ]
Cosio, F. [1 ]
Lager, D. J. [2 ]
Stegall, M. D. [3 ]
机构
[1] Mayo Clin & Mayo Fdn, Dept Nephrol & Internal Med, Rochester, MN 55905 USA
[2] Mayo Clin & Mayo Fdn, Dept Lab Med & Pathol, Div Anat Pathol, Rochester, MN USA
[3] Mayo Clin & Mayo Fdn, Dept Surg, Div Transplant Surg, Rochester, MN USA
关键词
antibody-mediated rejection; anti-HLA antibodies; donor-specific antibodies; kidney transplantation; transplant glomerulopathy;
D O I
10.1111/j.1600-6143.2008.02262.x
中图分类号
R61 [外科手术学];
学科分类号
摘要
Improvements in anti-HLA antibody detection and diagnostic criteria have increased recognition of antibody-mediated rejection (AMR) following renal transplantation. Therapy of acute AMR is directed toward rapidly lowering circulating donor-specific antibody (DSA) activity. Despite reversal of acute renal dysfunction, however, antibody-secreting plasma cells in spleen and bone marrow are not depleted by treatment and circulating DSA commonly remains detectable in peripheral blood. Sequential ultrastructural studies of renal allografts during acute AMR show progression of microvascular endothelial abnormalities from necrosis and apoptosis to glomerular and peritubular capillary basement membrane duplication, termed transplant glomerulopathy (TG), a manifestation of chronic AMR. Additionally, long-term exposure to anti-HLA antibodies (particularly against class II antigens) is associated with shortened allograft survival and TG even in the absence of documented acute AMR. The association of TG with prior acute AMR and with circulating DSA provides evidence that antibody-mediated allograft injury exists as a spectrum of renal injury. Although effective therapy is available for acute AMR, allografts remain at risk for chronic AMR and shortened survival. The optimum approach to treatment for chronic AMR remains to be determined.
引用
收藏
页码:1367 / 1373
页数:7
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