The characteristics of this glomerulopathy are:
- Endothelial cell hypertrophy or necrosis
- Narrowing or obliteration of capillary lumens
- Fibrillar deposits in glomerular capillaries
- Mild segmental hypercelbularity
- Mononuclear cell infiltration without tubular changes
- IF revealed deposition of IgG, IgM, and C3 along the glomerular basement membrane and within the mesangium
- One specimen, anti-CMV antibody staining was observed within glomerular capillaries
- No viral inclusions were found on EM.
Others reported different types of lesions like cryoglobulinemic necrotizing GN or immunotactoid glomerulopathy. The association in those cases were made based on temporal relationship between the appearance of CMV antigenemia and the lesion.
The authors suggested that the glomerular changes represented a form of acute transplant gbomerulopathy resulting from antiendothelial antibody injury or a protracted, early, or unresolved form of acute vascular rejection. Furthermore, Harmon et al. showed that this glomerulopathy occurred in only seven of 56 renal allograft recipients with a clinical diagnosis of CMV disease. Three of the seven patients with this lesion were not even viremic. Anderson et al., using immunohistochemistry and in situ hybridization on 15 biopsy specimens from viremic renal allograft recipients with glomerulopathy, found no evidence of CMV antigens or DNA.
Our case is different because there are viral inclusions in the epithelial but also in the endothelial cells with some swelling noticed by our famous pathologist. There was no associated glomerular inflammation and C4d staining was negative. The lesion was called CMV glomerulitis but it is obviously different from the CMV glomerulopathy described by Dr. Rubin in his NEJM paper. Patient was treated with Cidofovir. Her creatinine improved to baseline and her lesions improved on a subsequent follow up kidney biopsy. Since than, many reports described the same lesions associated with CMV infection, including a report in AJKD. The CMV glomerulitis similar to our case progressed to collapsing FSGS. The lack of proteinuria before transplantation supported the contention that the collapsing glomerulopathy arose de novo rather than being recurrent.