Late-onset BK viral nephropathy in a kidney transplant recipient.

BK polyoma viral infection occurs as an asymptomatic infection in a high proportion of normal hosts without obvious sequelae. In the kidney transplant population, the virus is reactivated because of reduced immunity and, if not appropriately managed, can lead to BK viral nephropathy, which has emerged as a common cause of acute kidney injury and progressive chronic kidney disease in renal transplant recipients. BK viremia almost always occurs during the first 2 years after transplantation, when immunosuppressive therapy is high, or at other periods when immunosuppression is intensified. BK viremia is now detected by routine screening of transplant patients for the first few years, and BK viral nephropathy is considered to be high in the differential diagnosis of acute kidney injury in recently transplanted patients. We report a case of BK viral nephropathy developing 10 years after transplantation and present the challenges of managing advanced disease.

Acute transplant glomerulopathy is associated with antibody-mediated rejection and poor graft outcome.

Transplant glomerulopathy (TG) is traditionally considered to be a chronic entity. However, in our practice we observed patients who presented with features of TG as early as 14 days posttransplantation. We investigated the clinicopathological features of these cases. During a 4-year period, all patients with acute rejection were identified. Charts were reviewed to identify patients with antibody-mediated rejection and biopsy features of TG within 6 months posttransplantation. Three patients met the above-mentioned criteria. All of them had diffuse margination of inflammatory cells in peritubular capillaries in the setting of acute renal failure or delayed graft function. Monocyte (CD68-positive) margination in peritubular capillaries was a common feature. All 3 patients had donor-specific antibodies and features suggestive of antibody-mediated rejection. C4d stain in peritubular capillaries was focal and mild or absent in serial biopsies. Occlusive endothelial swelling of glomerular capillary loops (endotheliosis) preceded TG. None of the patients had evidence for other causes of similar glomerular changes in a transplant, such as calcineurin inhibitor toxicity, ischemia, hepatitis C, or immune complex glomerulonephritis. They did not have other biopsy features of chronicity when TG appeared and as it progressed. TG can occur as an acute phenomenon. We propose that endotheliosis is a more accurate and specific precursor of TG than mere glomerulitis. These cases of acute TG may represent a form of antibody-mediated rejection associated with proteinuria and poor response to treatment.

Vascular access malfunction due to upper extremity embolization in dialysis patients.

Acute occlusions of arteries such as those of the cerebral and peripheral circulation are usually due to thrombotic or embolic events. Emboli have not been previously reported to cause arteriovenous (AV) dialysis access malfunction. We describe in this report three patients with end-stage renal disease (ESRD) and atrial fibrillation (Afib) who developed acute ischemia of an arteriovenous access-bearing extremity due to embolization. The clinical manifestations mimicked thrombotic events, but the presence of symptoms and signs of limb ischemia distinguished these cases clinically. A timely diagnosis followed by an appropriate intervention can lead to limb and access salvage.