As acute rejection rates continue to fall, causes of late allograft loss, such as transplant glomerulopathy (TG), become increasingly important. TG should spring to mind when you encounter a renal transplant recipient who develops heavy proteinuria and progressive allograft failure, usually late post-transplant. The clinical presentation overlaps with that of chronic allograft nephropathy, although proteinuria tends to be greater in TG and patients are likely to have a history of donor-specific anti-HLA antibodies. The pathogenesis is believed to relate to the presence of these donor-specific antibodies, which are often often anti-HLA Class II. These may wax and wane in concentration and, as a result, may not be detected on a single assay but repeat testing is usually successful. C4d staining is typically negative.
Various immunosupressive regimens have been tried, but none are known to be effective. Progressive graft failure and return to dialysis is the usual outcome. Finally, the increasing use of protocol biopsy informs us that ultrastructural changes that predate the TG lesion develop within the first months post-transplant and in apparently well-functioning kidneys.