Assessment of the Banff Working Group classification of definitive BK polyomavirus nephropathy.

Polyomavirus associated nephropathy (PyVAN) continues to be a burden in renal transplantation leading to allograft insufficiency or graft failure. A presumptive diagnosis of PyVAN is made based on the presence of BK polyomavirus in patients' plasma; however, kidney biopsy remains the gold standard to establish a definitive diagnosis. The Banff Working Group on PyVAN proposed a novel classification of definitive PyVAN based on polyomavirus replication/load level and the extent of interstitial fibrosis. The aim of our study was to test the newly defined classes of PyVAN using independent cohorts of 124 kidney transplant patients with PyVAN with respect to the initial presentation and outcome, and to compare our analysis to that previously reported. Detailed analysis of our cohort revealed that the proposed classification of PyVAN did not stratify or identify patients at increased risk of allograft failure. Specifically, while class 3 was associated with the worst prognosis, there was no significant difference between the outcomes in classes 1 and 2. We also found that the timing post-transplantation and inflammation in areas of interstitial fibrosis and tubular atrophy might be additional factors contributing to an unfavorable allograft outcome in patients with PyVAN.

Transplantation With APOL1 Risk Variant Kidney May Be Associated With Lifetime Risk for Recurrence of Focal Segmental Glomerulosclerosis: A Case Report and Review of Literature.

The APOL1 gene mutation is increasingly recognized as an import factor in living kidney donation. APOL1 gene variants prevalent in the African American population have been associated with increased risk of glomerulopathy. Shorter allograft survival is seen in transplants from donors who had 2 risk APOL1 gene alleles. In the early posttransplant period, kidneys with 2 risk alleles of APOL1 had higher risk of graft loss compared to 1 or 0 risk alleles, but by year 4 of transplant it was almost similar. The authors have suggested that recipients of kidney transplants with 2 risk alleles may only be at risk for kidney failure during the early initial period. We present here a case of a patient with 2 risk APOL1 alleles who received renal transplant from her identical twin and developed glomerulopathy 18 years after the transplant. No case of APOL1-associated recurrent glomerulonephritis has been described in a recipient after 10 years. This suggests that the risk of recurrence of glomerulopathy in allograft transplants with 2 risk allele variants may not be limited to the initial post-transplant period; rather, it may be a lifetime risk.