The diagnostic and therapeutic dilemma of the co-existence of BK virus nephropathy with acute rejection - an experience from a single Centre and review of the literature.

INTRODUCTION: BKV nephropathy (BKVN) is one of the major causes of graft loss with the advent of potent immunosuppressive drugs. The literature on the co-existence of acute rejection (AR) and BKVN is scarce. MATERIALS AND METHODS: This is a single-center retrospective analysis, where the allograft biopsies of patients transplanted between 2011 and 2021 were reviewed. The biopsies, which showed evidence of coexistent AR and BKVN, were included. In addition, demographic profiles, clinical presentation, treatment details, response to therapy, and follow-up were analyzed. RESULTS: Out of 1175 live transplants done between January 2011 and March 2021, 49 had BKVN representing 4.17%. Only seven patients (0.59%) had coexistent BKVN with AR. The mean serum creatinine at presentation was 2.3 mg/dl. The mean duration to diagnosis from transplant was seven months (range 3-22 months). All had significant viremia at presentation (17450-4,750,000 copies/ml). All biopsies showed type 1 inclusion bodies with SV40 positivity except one. Coexistent acute T cell-mediated rejection (TCMR) was found in five and acute ABMR in two patients. Three patients received pulse IV methylprednisolone, five received 2 g/kg IVIG, two received plasma exchange as upfront therapies. Maintenance immunosuppression reduction was made in all. Viremia clearance was noted at a mean duration of 3.5 months. However, three patients lost their grafts on follow-up. Four had stable graft function with a mean serum creatinine of 1.54 mg/dl. CONCLUSION: Intensifying immunosuppression to treat AR followed by a reduction in maintenance immunosuppression and IVIG and antiviral therapies seems better strategy and showed good long-term graft survival in patients with coexistent BKVN and AR.

Evanescing renal allograft cortical necrosis from living donor renal transplantation: A lesson learned over two decades.

BACKGROUND: Renal graft cortical necrosis (GCN) is a catastrophic cause of graft failure. We evaluated the incidence, causes, management, and outcome of GCN across two decades from our center. METHODS: This is a retrospective analysis of transplant patients who had biopsy-proven GCN transplanted between 2000 and 2020. The clinical details, immunological workup, induction, maintenance regimen, causes of cortical necrosis, and the outcomes were compared between the first period 2000-2012, and the second period 2013-2020, when Flow cytometric and Luminex based crossmatch were included in the workup plan. RESULTS: Among 2333 live ABO-compatible renal transplants, 37 (0.015%) patients (36 patients between 2000 and 2012 and 1 between 2013 and 2020) developed GCN (60% had diffuse and 40% patchy GCN) at a median of 8 days after transplantation.Twenty-six (60%) received ATG, 4 received plasmapheresis and ATG (10.8%) as antirejection therapy. The cyclosporine-based regimen was associated with a higher risk of GCN (RR 2.54; 95% CI 1.26 to 5.12, p = 0.009), whereas tacrolimus-based therapy had a lower risk (RR 0.39; 95% CI 0.19 to 0.79, p = 0.009). The introduction of flow cytometry and DSA assay has significantly decreased the incidence of acute rejection and GCN. Only one patient had GCN during the 2013-2020 period because of graft's mucormycosis. Twenty-five (67.56%) patients had no recovery, and 12 (32.43%) had partial recovery of graft function. CONCLUSION: GCN is mainly associated with rejection, and cyclosporin-based maintenance regimen had a higher incidence. The remarkable decrease in GCN after 2012 onwards could be attributed to the use of Flowcytometry, Luminex-based DSA assays, and tacrolimus-based regimens.