A young man who had an identical twin donor was recently transplanted. The cause of end-stage disease was IgA nephropathy. The donor had no renal dysfunction or proteinuria. There was no demonstrable HLA mismatch. The panel reactive antibody (PRA) and T- as well as B-cell cross match tests were negative. The post-transplant course was unremarkable. Tacrolimus and MMF-based immunosuppression was maintained until short tandem repeat analysis confirmed genetic identity between donor and recipients.
A 3-month protocol biopsy was performed. It showed no interstitial inflammation, tubulitis, glomerulitis, or peritubular capillaritis. C4d staining was negative. There was no interstitial fibrosis, interstitial fibrosis, or arteriosclerosis. The glomeruli looked unremarkable (Fig 1):
However, immunofluorescence and electron microscopic examination showed changes of early IgA nephropathy (Fig 2 and 3):
It has been decided to maintain the patient on 5 mg prednisone. A 12-month protocol biopsy will be performed to determine if the disease progresses. Meanwhile, it has been decided to offer no specific therapy.
It is likely that the biopsy findings represent an early stage of recurrent IgA nephropathy. However, we may also be simply detecting asymptomatic disease in the twin donor. Further follow-up will help differentiate these two possibilities.
This case illustrates how transplants from identical twins can develop immune-mediated diseases that do not fall into the category of rejection. Recurrent glomerulonephritis and death due to a cardiovascular event are the most common causes of graft loss after transplantation between identical twins.
– Post prepared by Parmjeet Randhawa, AJKDBlog Contributor.