BK Breaks the Rules: AKI Due to BK Virus in a Native Kidney

Introduction: BK virus is a polyoma virus, that although most people contract during childhood, has been described to be pathogenic in the context of robust transplant immunosuppression. Although uncommon, there are cases of human polyoma BK virus being nephrotoxic in native kidneys, especially in nontransplant patients on systemic immunosuppression. This case highlights native kidney BK nephropathy in a patient who received Upadacitinib for Crohn’s disease. Case Description: 44 year-old female with a past medical history significant for Crohn's disease on Upadacitinib, hypertension and asthma initially presented with complaints of fatigue, watery diarrhea, nausea, vomiting and syncope and was found to have acute kidney injury. Her clinical course was further complicated by pancytopenia due to autoimmune myelofibrosis and left arm lichen simplex chronicus with epidermal necrosis. Initial laboratory findings were significant for hyponatremia, hypokalemia, hypocalcemia and hypophosphatemia and a creatinine of 6.44, up from a baseline of 0.72 six months prior. Urinalysis showed blood and proteinuria. UACR was 142 and UPCR was 0.84. Serologies for glomerulonephritis were unrevealing. CMV PCR was negative and BK PCR showed a viral load of 929000 Iu/ml. Renal biopsy was pursued and demonstrated Human Polyomavirus Nephritis, Banff Class 2 with moderate to marked interstitial fibrosis and tubular atrophy with 10% of overall tubules showing SV40 positive epithelial nuclei. Despite significant tubulointerstitial scarring, the global sclerosis did not exceed the reference limit. Despite medical management of electrolyte abnormalities and metabolic acidosis, persistent uremia led to initiation of hemodialysis while cidofovir was administered to treat the viral burden. Discussion: BK virus associated nephropathy is directly correlated to aggressive immune system suppression in the transplant domain. This icosahedral virus, which is transmissible through respiratory droplets, is associated with interstitial nephritis and direct cytopathy in the setting of transplantation. Upadacitinib is a JAK inhibitor and thus suppresses an inflammatory response. Yet, the virus has not been directly linked to Upacitinb in the literature until now. With BK viremia leading to acute renal failure such as in our case, it is reasonable to question whether the virus should be further investigated in non-transplant immunosuppression.