Faculty Bibliography

Antibody mediated injury to a renal allograft is biologically complex and is manifest by multiple phenotypes which appear to be defined by the extent and timing of the humoral response. Transplant glomerulopathy (tg) is the ultimate arbitrator of whether the injury becomes an enduring feature that limits the longevity of the allograft and it is the end stage lesion that unites the different phenotypes. For the last few decades the focus for treatment has been on removing or modulating donor specific antibody (DSA) with plasmapheresis and IVIg. This approach has been effective when the rejection is acute and the antibody production modest. Even under those circumstances tg will be present within a year of the antibody mediated rejection (ABMR) episode in nearly half of the allografts. Because IgG is distributed throughout the interstitium, the removal or inactivation of antibody is not immediate. While efforts are being made to manage DSA, the renal microcirculation remains vulnerable to the injurious effects of soluble DSA, especially antibodies that activate complement