Recurrent glomerulonephritis in the kidney allograft

Abstract

Renal transplantation is the preferred form of renal replacement therapy in patients who develop end-stage kidney disease (ESKD). Among the diverse etiologies of ESKD, glomerulonephritis is the third most common cause, behind hypertensive and diabetic kidney disease. Although efforts to prolong graft survival have improved over time with the advent of novel immunosuppression, recurrent glomerulonephritis remains a major threat to renal allograft survival despite concomitant immunosuppression. As a result, clinical expertise, early diagnosis and intervention will help identify recurrent disease and facilitate prompt treatment, thus minimizing graft loss, resulting in improved outcomes. In this review, we highlight the clinicopathologcal characteristics of certain glomerular diseases that recur in the renal allograft.

CMV‐associated collapsing focal segmental glomerulosclerosis after kidney transplant in a pediatric patient

“…Their patient's kidney biopsy demonstrated collapsing features in three of nine sampled glomeruli, and similarly to our patient, it was negative for CMV immunostaining and did not show viral inclusions 6 . Negative CMV staining and the absence of inclusion bodies raise the possibility of an immune‐mediated rather than a viral‐mediated mechanism for CMV‐induced collapsing FSGS, which is also suggested by Patel et al 6,12 Additionally, the kidney transplant biopsy did not reveal a recurrence of lupus nephritis as the cause of nephrosis, consistent with prior studies demonstrating a low incidence of lupus nephritis recurrence in graft tissue 11,13 …”

“…6 Negative CMV staining and the absence of inclusion bodies raise the possibility of an immune-mediated rather than a viral-mediated mechanism for CMV-induced collapsing FSGS, which is also suggested by Patel et al 6,12 Additionally, the kidney transplant biopsy did not reveal a recurrence of lupus nephritis as the cause of nephrosis, consistent with prior studies demonstrating a low incidence of lupus nephritis recurrence in graft tissue. 11,13 This proposed T-cell mediated mechanism is supported by our patient's biopsy results which demonstrated acute T-cell mediated rejection changes but had negative CMV viral staining. Other phenotypic switches, from IgA nephropathy to collapsing FSGS, are also reported after kidney transplantation in a retrospective study by Karthikeyan et al; however, it is unknown whether CMV induced the immune response in their study due to the lack of data on donor CMV status.…”