Abstract
Antibody-mediated rejection (AMR) is highly detrimental to the prolonged survival of transplanted kidneys. C4d has been regarded as a footprint of AMR tissue damage, and the introduction of C4d staining in daily clinical practice aroused an ever-increasing interest in the role of antibody-mediated mechanisms in allograft rejection. Despite the general acceptance of the usefulness of C4d in the identification of acute AMR, the data for C4d staining in chronic AMR is variable. The presence of C4d in the majority of the biopsies with features of chronic antibody-mediated rejection is reported, but this rejection without C4d staining is observed as well, suggesting that C4d is specific but not sensitive. Further studies on AMR with positive C4d staining in biopsy specimens are really important, as well as the study of novel routine markers that may participate in the pathogenesis of this process.
Highlights
In renal transplant, the allograft is responsible for triggering many innate and adaptive immune mechanisms, either mediated by cells, such as macrophages and lymphocytes, or by soluble components, such as antibodies and the complement system, which can lead to graft rejection [1].According to the Banff criteria [2], rejection may be mediated by cells or by antibodies and may be acute or chronic
C4d deposition without Antibody-mediated rejection (AMR) has been observed even in transplant glomerulopathy (TG), which is regarded as a chronic AMR and is characterized by proteinuria and loss of renal function over time, culminating in graft loss [5]
This review aimed to identify the role of C4d in episodes of AMR, especially in cases of TG
Summary
The allograft is responsible for triggering many innate and adaptive immune mechanisms, either mediated by cells, such as macrophages and lymphocytes, or by soluble components, such as antibodies and the complement system, which can lead to graft rejection [1]. According to the Banff criteria [2], rejection may be mediated by cells or by antibodies and may be acute or chronic. The morphological diagnosis of AMR consists of various morphological changes together with C4d deposition in the microcirculation of the allograft. C4d deposition without AMR has been observed even in transplant glomerulopathy (TG), which is regarded as a chronic AMR and is characterized by proteinuria and loss of renal function over time, culminating in graft loss [5]. This review aimed to identify the role of C4d in episodes of AMR, especially in cases of TG
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