Polyomavirus nephropathy (PVN) is a common viral infection of renal allografts, with biopsy-proven incidence of approximately 5%. A generally accepted morphologic classification of definitive PVN that groups histologic changes, reflects clinical presentation, and facilitates comparative outcome analyses is lacking. Here, we report a morphologic classification scheme for definitive PVN from the Banff Working Group on Polyomavirus Nephropathy, comprising nine transplant centers in the United States and Europe. This study represents the largest systematic analysis of definitive PVN undertaken thus far. In a retrospective fashion, clinical data were collected from 192 patients and correlated with morphologic findings from index biopsies at the time of initial PVN diagnosis. Histologic features were centrally scored according to Banff guidelines, including additional semiquantitative histologic assessment of intrarenal polyomavirus replication/load levels. In-depth statistical analyses, including mixed effects repeated measures models and logistic regression, revealed two independent histologic variables to be most significantly associated with clinical presentation: intrarenal polyomavirus load levels and Banff interstitial fibrosis ci scores. These two statistically determined histologic variables formed the basis for the definition of three PVN classes that correlated strongest with three clinical parameters: presentation at time of index biopsy, serum creatinine levels/renal function over 24 months of follow-up, and graft failure. The PVN classes 1-3 as described here can easily be recognized in routine renal biopsy specimens. We recommend using this morphologic PVN classification scheme for diagnostic communication, especially at the time of index diagnosis, and in scientific studies to improve comparative data analysis.

Negative EM and absence of decoy cells could be used as broad indicators of a response to intervention. However, measurement of BK virus DNA level provided a wider dynamic range and could be a better choice for determining the extent of viral control.

Collapsing glomerulopathy has increasingly been recognised in patients with conditions other than HIV. The non-HIV form of collapsing glomerulopathy generally shows little response to standard therapies. We describe a 12-year-old girl with a pre-existing diagnosis of systemic lupus erythematosus presenting with renal failure. A renal biopsy gave the histological diagnosis of collapsing glomerulopathy with evidence of "full-house" immunostaining. We propose collapsing glomerulopathy in her case, as no other cause was found was secondary to systemic lupus erythematosus. The immunophenotype of her podocytes suggested a partial de-differentiation that might have been important in her partial response to immunosuppression.

The renal complications of dengue virus infection cover a wide spectrum of manifestations from acute kidney injury to glomerular injury with nephritic/nephrotic syndrome. Majority of cases remain symptom free and show full recovery. We present a 61-year-old previously healthy male who developed a pyrexial illness with haemolytic anaemia that was diagnosed on the basis of a positive serological test as a case of dengue fever. He received supportive treatment and showed general recovery except for his renal dysfunction that showed persistent proteinuria at 14 gm/24 hours. A kidney biopsy revealed membranoproliferative glomerulonephritis type 1 (MPGN-l). Complete remission was achieved by steroids and mycophenolate mofetil therapy. We provide convincing biopsy evidence that dengue virus is yet another viral cause of MPGN-l and also document its successful management with mycophenolate mofetil and steroids therapy.